Pub Date : 2024-10-05DOI: 10.1016/j.ijheh.2024.114472
Minjin Peng , Yachen Li , Jing Wu , Yi Zeng , Yao Yao , Yunquan Zhang
<div><h3>Background</h3><div>Cohort evidence linking increased mortality with airborne fine particulate matter (PM<sub>2.5</sub>, particulate matter [PM] with aerodynamic diameter ≤2.5 μm) exposure was extensively validated worldwide. Nevertheless, long-term survival associated with submicron particulate matter (PM<sub>1</sub>, PM with aerodynamic diameter ≤1 μm) exposure remained largely unstudied, particularly in highly exposed populations.</div></div><div><h3>Methods</h3><div>We performed a population-based investigation involving 86844 adults aged 16+ years from 3 national dynamic cohorts spanning from 2005 to 2018. Residential annual exposure to PM<sub>1</sub> and PM<sub>2.5</sub> was assigned for each follow-up year using satellite-derived spatiotemporal estimates at a 1-km<sup>2</sup> resolution. The concentration of PM<sub>1-2.5</sub> (PM with aerodynamic diameter between 1 and 2.5 μm) was calculated by subtracting PM<sub>1</sub> from PM<sub>2.5</sub>. Time-independent Cox proportional hazards regression models were applied to assess the associations of all-cause mortality with long-term exposure to size-specific particles. To investigate the effect of PM<sub>1</sub> on PM<sub>2.5</sub>-mortality associations, we categorized participants into low, medium, and high groups based on PM<sub>1</sub>/PM<sub>2.5</sub> ratio and examined the risk of PM<sub>2.5</sub>-associated mortality in each stratum. Effect modifications were checked via subgroup analyses.</div></div><div><h3>Results</h3><div>A total of 18722 deaths occurred during 497069.2 person-years of follow-up (median 5.7 years). Participants were exposed to an average annual concentration of 31.8 μg/m³ (range: 7.6–66.8 μg/m³) for PM<sub>1</sub>, 56.3 μg/m³ (range: 19.8–127.2 μg/m³) for PM<sub>2.5</sub>, and 24.5 μg/m³ (range: 7.3–60.3 μg/m³) for PM<sub>1-2.5</sub>. PM<sub>1</sub>, PM<sub>2.5</sub>, and PM<sub>1-2.5</sub> were consistently associated with elevated mortality risks, with a hazard ratio (HR) of 1.029 (95% confidence interval [CI]: 1.013–1.046), 1.014 (95% CI: 1.005–1.023), and 1.019 (95% CI: 1.001–1.038) for each 10-μg/m<sup>3</sup> increase in exposure, respectively. Compared with low (HR = 0.986, 95% CI: 0.967–1.004) and medium (HR = 1.015, 95% CI: 1.002–1.029) PM<sub>1</sub>/PM<sub>2.5</sub> ratio groups, PM<sub>2.5</sub>-related risk of mortality was more pronounced in high PM<sub>1</sub>/PM<sub>2.5</sub> ratio stratum (HR = 1.041, 95% CI: 1.019–1.064). Greater risks of mortality associated with size-specific particles were found among the elderly (>80 years old), southeastern participants, and those living in warmer areas.</div></div><div><h3>Conclusions</h3><div>This study demonstrated that long-term exposure to PM<sub>1</sub>, PM<sub>2.5</sub>, and PM<sub>1-2.5</sub> was associated with heightened mortality, and PM<sub>1</sub> may play a predominant role in PM<sub>2.5</sub>-induced risk. Our results emphasized the population health implications of establishing amb
{"title":"Exposure to submicron particulate matter and long-term survival: Cross-cohort analysis of 3 Chinese national surveys","authors":"Minjin Peng , Yachen Li , Jing Wu , Yi Zeng , Yao Yao , Yunquan Zhang","doi":"10.1016/j.ijheh.2024.114472","DOIUrl":"10.1016/j.ijheh.2024.114472","url":null,"abstract":"<div><h3>Background</h3><div>Cohort evidence linking increased mortality with airborne fine particulate matter (PM<sub>2.5</sub>, particulate matter [PM] with aerodynamic diameter ≤2.5 μm) exposure was extensively validated worldwide. Nevertheless, long-term survival associated with submicron particulate matter (PM<sub>1</sub>, PM with aerodynamic diameter ≤1 μm) exposure remained largely unstudied, particularly in highly exposed populations.</div></div><div><h3>Methods</h3><div>We performed a population-based investigation involving 86844 adults aged 16+ years from 3 national dynamic cohorts spanning from 2005 to 2018. Residential annual exposure to PM<sub>1</sub> and PM<sub>2.5</sub> was assigned for each follow-up year using satellite-derived spatiotemporal estimates at a 1-km<sup>2</sup> resolution. The concentration of PM<sub>1-2.5</sub> (PM with aerodynamic diameter between 1 and 2.5 μm) was calculated by subtracting PM<sub>1</sub> from PM<sub>2.5</sub>. Time-independent Cox proportional hazards regression models were applied to assess the associations of all-cause mortality with long-term exposure to size-specific particles. To investigate the effect of PM<sub>1</sub> on PM<sub>2.5</sub>-mortality associations, we categorized participants into low, medium, and high groups based on PM<sub>1</sub>/PM<sub>2.5</sub> ratio and examined the risk of PM<sub>2.5</sub>-associated mortality in each stratum. Effect modifications were checked via subgroup analyses.</div></div><div><h3>Results</h3><div>A total of 18722 deaths occurred during 497069.2 person-years of follow-up (median 5.7 years). Participants were exposed to an average annual concentration of 31.8 μg/m³ (range: 7.6–66.8 μg/m³) for PM<sub>1</sub>, 56.3 μg/m³ (range: 19.8–127.2 μg/m³) for PM<sub>2.5</sub>, and 24.5 μg/m³ (range: 7.3–60.3 μg/m³) for PM<sub>1-2.5</sub>. PM<sub>1</sub>, PM<sub>2.5</sub>, and PM<sub>1-2.5</sub> were consistently associated with elevated mortality risks, with a hazard ratio (HR) of 1.029 (95% confidence interval [CI]: 1.013–1.046), 1.014 (95% CI: 1.005–1.023), and 1.019 (95% CI: 1.001–1.038) for each 10-μg/m<sup>3</sup> increase in exposure, respectively. Compared with low (HR = 0.986, 95% CI: 0.967–1.004) and medium (HR = 1.015, 95% CI: 1.002–1.029) PM<sub>1</sub>/PM<sub>2.5</sub> ratio groups, PM<sub>2.5</sub>-related risk of mortality was more pronounced in high PM<sub>1</sub>/PM<sub>2.5</sub> ratio stratum (HR = 1.041, 95% CI: 1.019–1.064). Greater risks of mortality associated with size-specific particles were found among the elderly (>80 years old), southeastern participants, and those living in warmer areas.</div></div><div><h3>Conclusions</h3><div>This study demonstrated that long-term exposure to PM<sub>1</sub>, PM<sub>2.5</sub>, and PM<sub>1-2.5</sub> was associated with heightened mortality, and PM<sub>1</sub> may play a predominant role in PM<sub>2.5</sub>-induced risk. Our results emphasized the population health implications of establishing amb","PeriodicalId":13994,"journal":{"name":"International journal of hygiene and environmental health","volume":"263 ","pages":"Article 114472"},"PeriodicalIF":4.5,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142383065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-05DOI: 10.1016/j.ijheh.2024.114473
Maxine Pepper , Poliana Rebouças , Ila R. Falcão , Nuria Sanchez Clemente , Rachel Lowe , Rochelle Schneider , Julia M. Pescarini , Gervásio F. dos Santos , Roberto FS. Andrade , Taísa R. Cortes , Otavio T. Ranzani , Elizabeth B. Brickley , Mauricio L. Barreto , Enny S. Paixao
Background
Pregnancy represents a critical window of vulnerability to the harmful effects of air pollution on health. However, long-term consequences such as risk of having lower respiratory tract infections (LRTIs) are less explored. This systematic review aims to synthesize previous research on prenatal exposure to ambient (outdoor) air pollution and LRTIs in childhood and adolescence.
Methods
We systematically searched Embase, MEDLINE, Web of Science Core Collection, CINAHL, and Global Health up to May 17, 2024. We included peer-reviewed publications of studies which investigated the association between prenatal exposure to ambient air pollution and LRTIs up to the age of 19. We excluded conference abstracts, study protocols, review articles, and grey literature. Screening and data extraction was conducted by two reviewers independently. We used the Office of Health Assessment and Translation tool to assess risk of bias and conducted a narrative synthesis.
Results
The search yielded 6056 records, of which 16 publications describing 12 research studies were eligible for the synthesis. All studies were conducted in high- or upper-middle-income countries in Europe or Asia. Half (6) of the studies focused on LRTIs occurring within the first three years of life, and the others also included LRTIs in older children (up to age 14). Air pollutants investigated included nitrogen dioxide, sulphur dioxide, particulate matter (PM2.5: diameter ≤2.5 μm and PM10: diameter ≤10 μm), carbon monoxide, ozone, and benzene. Findings on a potential association between prenatal ambient air pollution exposure and LRTIs were inconclusive, without a clear and consistent direction. There was some suggestion of a positive association with prenatal PM2.5 exposure. The small number of studies identified, their poor geographical representation, and their methodological limitations including concerns for risk of bias preclude more definitive conclusions.
Conclusion
The available published evidence is insufficient to establish whether prenatal exposure to ambient air pollution increases risk of LRTIs in children and adolescents. With many populations exposed to high levels of air pollution, there is an urgent need for research in more diverse settings, more transparent reporting of methods, and exploring how, when, and for whom prenatal exposure to ambient air pollution leads to the greatest health risks.
{"title":"Prenatal exposure to ambient air pollution and subsequent risk of lower respiratory tract infections in childhood and adolescence: A systematic review","authors":"Maxine Pepper , Poliana Rebouças , Ila R. Falcão , Nuria Sanchez Clemente , Rachel Lowe , Rochelle Schneider , Julia M. Pescarini , Gervásio F. dos Santos , Roberto FS. Andrade , Taísa R. Cortes , Otavio T. Ranzani , Elizabeth B. Brickley , Mauricio L. Barreto , Enny S. Paixao","doi":"10.1016/j.ijheh.2024.114473","DOIUrl":"10.1016/j.ijheh.2024.114473","url":null,"abstract":"<div><h3>Background</h3><div>Pregnancy represents a critical window of vulnerability to the harmful effects of air pollution on health. However, long-term consequences such as risk of having lower respiratory tract infections (LRTIs) are less explored. This systematic review aims to synthesize previous research on prenatal exposure to ambient (outdoor) air pollution and LRTIs in childhood and adolescence.</div></div><div><h3>Methods</h3><div>We systematically searched Embase, MEDLINE, Web of Science Core Collection, CINAHL, and Global Health up to May 17, 2024. We included peer-reviewed publications of studies which investigated the association between prenatal exposure to ambient air pollution and LRTIs up to the age of 19. We excluded conference abstracts, study protocols, review articles, and grey literature. Screening and data extraction was conducted by two reviewers independently. We used the Office of Health Assessment and Translation tool to assess risk of bias and conducted a narrative synthesis.</div></div><div><h3>Results</h3><div>The search yielded 6056 records, of which 16 publications describing 12 research studies were eligible for the synthesis. All studies were conducted in high- or upper-middle-income countries in Europe or Asia. Half (6) of the studies focused on LRTIs occurring within the first three years of life, and the others also included LRTIs in older children (up to age 14). Air pollutants investigated included nitrogen dioxide, sulphur dioxide, particulate matter (PM<sub>2.5</sub>: diameter ≤2.5 μm and PM<sub>10</sub>: diameter ≤10 μm), carbon monoxide, ozone, and benzene. Findings on a potential association between prenatal ambient air pollution exposure and LRTIs were inconclusive, without a clear and consistent direction. There was some suggestion of a positive association with prenatal PM<sub>2.5</sub> exposure. The small number of studies identified, their poor geographical representation, and their methodological limitations including concerns for risk of bias preclude more definitive conclusions.</div></div><div><h3>Conclusion</h3><div>The available published evidence is insufficient to establish whether prenatal exposure to ambient air pollution increases risk of LRTIs in children and adolescents. With many populations exposed to high levels of air pollution, there is an urgent need for research in more diverse settings, more transparent reporting of methods, and exploring how, when, and for whom prenatal exposure to ambient air pollution leads to the greatest health risks.</div></div><div><h3>PROSPERO registration number</h3><div>CRD42023407689.</div></div>","PeriodicalId":13994,"journal":{"name":"International journal of hygiene and environmental health","volume":"263 ","pages":"Article 114473"},"PeriodicalIF":4.5,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-05DOI: 10.1016/j.ijheh.2024.114478
Jenita Cangola , Felix K. Abagale , Samuel J. Cobbina , Richard A. Osei
The use of wastewater for non-potable purposes is an important alternative for addressing water scarcity, especially in developing regions. However, minimizing the risks, particularly those associated with emerging contaminants that may induce resistance among pathogens in wastewater, is crucial. This study assessed the occurrence of antibiotic-resistant bacteria in untreated wastewater used for agricultural purposes and evaluated the quantifiable health risks associated with this practice in Tamale, Ghana. The resistance of some Enterobacteriaceae, such as E. coli, Klebsiella, and Salmonella-Shigella, to four commonly used antibiotics in Ghana was assessed using a conventional microbiological culture approach and the Kirby Bauer disk diffusion method. A Quantitative Microbial Risk Assessment (QMRA) was performed to estimate the health risks associated with two distinct scenarios of wastewater reuse: (1) accidental ingestion of contaminated wastewater and soil, and (2) consumption of vegetables irrigated with wastewater. This approach applied a Monte Carlo simulation based on 10,000 interactions and identified E. coli O157:H7 as the reference pathogen. Among Enterobacteriaceae, Klebsiella pneumoniae, Salmonella-Shigella and E. coli were isolated, in concentrations exceeding the limit recommended by the World Health Organization (103 CFU/100 ml). All the isolated bacteria were resistant to metronidazole (5 μg). Thirty-three per cent of Klebsiella pneumoniae isolates were intermediate/moderately susceptible, and all other bacteria were resistant to amoxicillin (30 μg). All Klebsiella pneumoniae and the majority of Salmonella-Shigella (69.8 %) isolates were resistant to trimethoprim-sulfamethoxazole (25 μg) and tetracycline (30 μg). When assessing health risks, the mean annual probability of infection associated with consuming vegetables irrigated with wastewater varied between 5.14 × 10−2 and 9.79 × 10−1 per person per year. Conversely, for the accidental ingestion scenario, the probability was 1.00 per person per year. In these scenarios, the probability of illness ranged from 1.29 × 10−2 to 2.4 × 10−1 and 2.5 × 10−1 per person per year. The health risks posed by these findings surpass the maximum threshold prescribed by the World Health Organization, thereby emphasizing the need for prompt mitigation strategies.
{"title":"Prevalence of antibiotic-resistant enterobacteriaceae in domestic wastewater and associated health risks in reuse practices","authors":"Jenita Cangola , Felix K. Abagale , Samuel J. Cobbina , Richard A. Osei","doi":"10.1016/j.ijheh.2024.114478","DOIUrl":"10.1016/j.ijheh.2024.114478","url":null,"abstract":"<div><div>The use of wastewater for non-potable purposes is an important alternative for addressing water scarcity, especially in developing regions. However, minimizing the risks, particularly those associated with emerging contaminants that may induce resistance among pathogens in wastewater, is crucial. This study assessed the occurrence of antibiotic-resistant bacteria in untreated wastewater used for agricultural purposes and evaluated the quantifiable health risks associated with this practice in Tamale, Ghana. The resistance of some Enterobacteriaceae, such as <em>E. coli, Klebsiella, and Salmonella-Shigella,</em> to four commonly used antibiotics in Ghana was assessed using a conventional microbiological culture approach and the Kirby Bauer disk diffusion method. A Quantitative Microbial Risk Assessment (QMRA) was performed to estimate the health risks associated with two distinct scenarios of wastewater reuse: (1) accidental ingestion of contaminated wastewater and soil, and (2) consumption of vegetables irrigated with wastewater. This approach applied a Monte Carlo simulation based on 10,000 interactions and identified <em>E. coli</em> O157:H7 as the reference pathogen. Among Enterobacteriaceae, <em>Klebsiella pneumoniae, Salmonella-Shigella</em> and <em>E. coli</em> were isolated, in concentrations exceeding the limit recommended by the World Health Organization (10<sup>3</sup> CFU/100 ml). All the isolated bacteria were resistant to metronidazole (5 μg). Thirty-three per cent of <em>Klebsiella pneumoniae</em> isolates were intermediate/moderately susceptible, and all other bacteria were resistant to amoxicillin (30 μg). All <em>Klebsiella pneumoniae</em> and the majority of <em>Salmonella-Shigella</em> (69.8 %) isolates were resistant to trimethoprim-sulfamethoxazole (25 μg) and tetracycline (30 μg). When assessing health risks, the mean annual probability of infection associated with consuming vegetables irrigated with wastewater varied between 5.14 × 10<sup>−2</sup> and 9.79 × 10<sup>−1</sup> per person per year. Conversely, for the accidental ingestion scenario, the probability was 1.00 per person per year. In these scenarios, the probability of illness ranged from 1.29 × 10<sup>−2</sup> to 2.4 × 10<sup>−1</sup> and 2.5 × 10<sup>−1</sup> per person per year. The health risks posed by these findings surpass the maximum threshold prescribed by the World Health Organization, thereby emphasizing the need for prompt mitigation strategies.</div></div>","PeriodicalId":13994,"journal":{"name":"International journal of hygiene and environmental health","volume":"263 ","pages":"Article 114478"},"PeriodicalIF":4.5,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142383066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Up to now, studies on environmental, climatic, socio-economic factors, and non-pharmacological interventions (NPI) show diverse associations, often contrasting, with COVID-19 spread or severity. Most studies used large-scale, aggregated data, with limited adjustment for individual factors, most of them focused on viral spread than severe outcomes. Moreover, evidence simultaneously evaluating variables belonging to different exposure domains is scarce, and none analysing their collective impact on an individual level.
Methods
Our population-based retrospective cohort study aimed to assess the comprehensive role played by exposure variables belonging to four different domains, environmental, climatic, socio-economic, and non-pharmacological interventions (NPI), on individual COVID-19-related risk of hospitalization and death, analysing data from all patients (no. 68472) tested positive to a SARS-CoV-2 swab in Modena Province (Northern Italy) between February 2020 and August 2021.
Using adjusted Cox proportional hazard models, we estimated the risk of severe COVID-19 outcomes, investigating dose-response relationships through restricted cubic spline modelling for hazard ratios.
Results
Several significant associations emerged: long-term exposure to air pollutants (NO2, PM10, PM2.5) was linked to hospitalization risk in a complex way and showed an increased risk for death; while humidity was inversely associated; temperature showed a U-shaped risk; wind speed showed a linear association with both outcomes. Precipitation increased hospitalization risk but decreased mortality. Socio-economic and NPI indices showed clear linear associations, respectively negative and positive, with both outcomes.
Conclusions
Our findings offer insights for evidence-based policy decisions, improving precision healthcare practices, and safeguarding public health in future pandemics. Refinement of pandemic response plans by healthcare authorities could benefit significantly.
{"title":"Environmental, climatic, socio-economic factors and non-pharmacological interventions: A comprehensive four-domain risk assessment of COVID-19 hospitalization and death in Northern Italy","authors":"Lucia Palandri , Cristiana Rizzi , Vittoria Vandelli , Tommaso Filippini , Alessandro Ghinoi , Giuliano Carrozzi , Gianfranco De Girolamo , Isabella Morlini , Paola Coratza , Enrico Giovannetti , Margherita Russo , Mauro Soldati , Elena Righi","doi":"10.1016/j.ijheh.2024.114471","DOIUrl":"10.1016/j.ijheh.2024.114471","url":null,"abstract":"<div><h3>Introduction</h3><div>Up to now, studies on environmental, climatic, socio-economic factors, and non-pharmacological interventions (NPI) show diverse associations, often contrasting, with COVID-19 spread or severity. Most studies used large-scale, aggregated data, with limited adjustment for individual factors, most of them focused on viral spread than severe outcomes. Moreover, evidence simultaneously evaluating variables belonging to different exposure domains is scarce, and none analysing their collective impact on an individual level.</div></div><div><h3>Methods</h3><div>Our population-based retrospective cohort study aimed to assess the comprehensive role played by exposure variables belonging to four different domains, environmental, climatic, socio-economic, and non-pharmacological interventions (NPI), on individual COVID-19-related risk of hospitalization and death, analysing data from all patients (no. 68472) tested positive to a SARS-CoV-2 swab in Modena Province (Northern Italy) between February 2020 and August 2021.</div><div>Using adjusted Cox proportional hazard models, we estimated the risk of severe COVID-19 outcomes, investigating dose-response relationships through restricted cubic spline modelling for hazard ratios.</div></div><div><h3>Results</h3><div>Several significant associations emerged: long-term exposure to air pollutants (NO<sub>2</sub>, PM<sub>10</sub>, PM<sub>2.5</sub>) was linked to hospitalization risk in a complex way and showed an increased risk for death; while humidity was inversely associated; temperature showed a U-shaped risk; wind speed showed a linear association with both outcomes. Precipitation increased hospitalization risk but decreased mortality. Socio-economic and NPI indices showed clear linear associations, respectively negative and positive, with both outcomes.</div></div><div><h3>Conclusions</h3><div>Our findings offer insights for evidence-based policy decisions, improving precision healthcare practices, and safeguarding public health in future pandemics. Refinement of pandemic response plans by healthcare authorities could benefit significantly.</div></div>","PeriodicalId":13994,"journal":{"name":"International journal of hygiene and environmental health","volume":"263 ","pages":"Article 114471"},"PeriodicalIF":4.5,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142376405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-03DOI: 10.1016/j.ijheh.2024.114475
Leire Luque-García , Gonzalo García-Baquero , Aitana Lertxundi , Wael K. Al-Delaimy , Jordi Julvez , Marisa Estarlich , Montserrat De Castro , Mònica Guxens , Manuel Lozano , Mikel Subiza-Pérez , Jesús Ibarluzea
Background
Epidemiological studies suggest that exposure to greenness during childhood may protect children from developing attention-deficit hyperactivity disorder (ADHD).
Objective
We analyzed the effect of both prenatal (pregnancy) and early childhood (4-5-year follow-up) residential greenness exposure and green space availability on ADHD symptoms during childhood (up to the age of 12 years) and further explored the potential mediating role of PM2.5 and physical activity in the association.
Methods
The study population included participants from the INfancia y Medio Ambiente (INMA) prospective birth cohort (Gipuzkoa, Sabadell, and Valencia). Average Normalized Difference Vegetation Index (NDVI) in buffers of 100-, 300- and 500-m around the residential addresses was used as an indicator of greenness, while green space availability was determined based on the presence of a major green space within 150-m from the residence. Childhood ADHD symptoms were assessed at the 6-8- and 10-12-year follow-ups using Conners Parents Rating Scale-Revised: Short Form.
Results
Although no association was found for the prenatal exposure period, increased early childhood NDVI inversely associated with the OR of clinically significant ADHD symptoms during the 6-8-year follow-up at the 100-m (OR 0.03, 95% CI: 0.003 to 0.44), 300-m (OR 0.04, 95% CI: 0.003 to 0.42) and 500-m (OR 0.08, 95% CI: 0.01 to 0.76) buffers, but exclusively in the context of direct effects. Additionally, the 10-12-year follow-up analysis found moderate to weak evidence of potential total and direct effects of NDVI at both 100- and 300-m buffers on inattention scores, as well as for NDVI at the 300-m buffer on ADHD index scores. The analysis did not reveal evidence of mediation through PM2.5 or physical activity.
Conclusions
The evidence suggests that early childhood greenness exposure may reduce the risk of developing ADHD symptoms later in childhood, and that this association is not mediated through PM2.5 and physical activity.
{"title":"Exploring the pathways linking prenatal and early childhood greenness exposure to attention-deficit/hyperactivity disorder symptoms during childhood: An approach based on robust causal inference","authors":"Leire Luque-García , Gonzalo García-Baquero , Aitana Lertxundi , Wael K. Al-Delaimy , Jordi Julvez , Marisa Estarlich , Montserrat De Castro , Mònica Guxens , Manuel Lozano , Mikel Subiza-Pérez , Jesús Ibarluzea","doi":"10.1016/j.ijheh.2024.114475","DOIUrl":"10.1016/j.ijheh.2024.114475","url":null,"abstract":"<div><h3>Background</h3><div>Epidemiological studies suggest that exposure to greenness during childhood may protect children from developing attention-deficit hyperactivity disorder (ADHD).</div></div><div><h3>Objective</h3><div>We analyzed the effect of both prenatal (pregnancy) and early childhood (4-5-year follow-up) residential greenness exposure and green space availability on ADHD symptoms during childhood (up to the age of 12 years) and further explored the potential mediating role of PM<sub>2.5</sub> and physical activity in the association.</div></div><div><h3>Methods</h3><div>The study population included participants from the <em>INfancia y Medio Ambiente</em> (INMA) prospective birth cohort (Gipuzkoa, Sabadell, and Valencia). Average Normalized Difference Vegetation Index (NDVI) in buffers of 100-, 300- and 500-m around the residential addresses was used as an indicator of greenness, while green space availability was determined based on the presence of a major green space within 150-m from the residence. Childhood ADHD symptoms were assessed at the 6-8- and 10-12-year follow-ups using Conners Parents Rating Scale-Revised: Short Form.</div></div><div><h3>Results</h3><div>Although no association was found for the prenatal exposure period, increased early childhood NDVI inversely associated with the OR of clinically significant ADHD symptoms during the 6-8-year follow-up at the 100-m (OR 0.03, 95% CI: 0.003 to 0.44), 300-m (OR 0.04, 95% CI: 0.003 to 0.42) and 500-m (OR 0.08, 95% CI: 0.01 to 0.76) buffers, but exclusively in the context of direct effects. Additionally, the 10-12-year follow-up analysis found moderate to weak evidence of potential total and direct effects of NDVI at both 100- and 300-m buffers on inattention scores, as well as for NDVI at the 300-m buffer on ADHD index scores. The analysis did not reveal evidence of mediation through PM<sub>2.5</sub> or physical activity.</div></div><div><h3>Conclusions</h3><div>The evidence suggests that early childhood greenness exposure may reduce the risk of developing ADHD symptoms later in childhood, and that this association is not mediated through PM<sub>2.5</sub> and physical activity.</div></div>","PeriodicalId":13994,"journal":{"name":"International journal of hygiene and environmental health","volume":"263 ","pages":"Article 114475"},"PeriodicalIF":4.5,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142376406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-28DOI: 10.1016/j.ijheh.2024.114470
Hao Zhao , Lanfei Jin , Kegui Huang , Kunhong Zhong , Yexinyi Zhou , Yang Xu , Qinheng Zhu , Jiena Zhou , Jun Tang , Qiong Luo , Jing Guo , Dan Zhang , Guangdi Chen
Previous studies have suggested that metal/metalloid (hereafter referred to as metal) exposure may influence placental growth by affecting gene expression in the placenta. However, no epidemiological studies have been conducted to validate the relationships between metals exposure, placental gene expression, and placental growth at the population level. This study aims to investigate these relationships based on Hangzhou birth cohort study II (HBCS-II). Totally, 1025 participants were derived from HBCS-II. Thirteen metals levels in the placenta were measured using inductively coupled plasma mass spectrometry. Placental growth characteristics were assessed, including placental weight, chorionic disc area, placental eccentricity, and distance from cord insertion site to the nearest edge of placenta (DCIEP). The relationships between metals exposure and placental growth characteristics were examined using the elastic net model combined unpenalized linear regression model. Placental gene expression levels were analyzed through RNA sequencing and real-time polymerase chain reaction (RT-qPCR), and mediation analysis was conducted to investigate whether placental gene expression could mediate the relationship between metal exposure and placental growth. Notably, the results showed that a unite increase in Ln-transformed cadmium (Cd) levels was associated with a reduction of 16.4 g [95% confidence interval (CI): 31.2, −1.5] in placental weight, 13.9 cm2 (95%CI: 20.0, −7.8) in chorionic disc area, and 0.3 cm (95%CI: 0.55, −0.06) in DCIEP. Through RNA sequencing followed by validation, significant associations were observed between placental Cd level and increased expression of placental genes, including TNFAIP2, OLAH, FLT4, SH3PXD2A, LIMCH1, BCL6, SLCO2A1, and CPSF1. Additionally, increased placental TNFAIP2, OLAH, FLT4, SH3PXD2A and LIMCH1 expression was linked to reduced placental weight. Moreover, SH3PXD2A was associated with decreased chorionic disc area. Mediation analysis showed that placental Cd level was associated with a 12.0 g (95%CI: 23.8, −2.7) decrease in placental weight mediated through the upregulation of FTL4 gene expression. The study provides evidence of the association between placental Cd exposure and decreased placental weight, and the FLT4 gene may play a mediating role in this relationship. Future experiment studies should be performed to validate the results.
{"title":"Associations between metal/metalloid exposure during pregnancy and placental growth characteristics: Findings from the Hangzhou birth cohort study II","authors":"Hao Zhao , Lanfei Jin , Kegui Huang , Kunhong Zhong , Yexinyi Zhou , Yang Xu , Qinheng Zhu , Jiena Zhou , Jun Tang , Qiong Luo , Jing Guo , Dan Zhang , Guangdi Chen","doi":"10.1016/j.ijheh.2024.114470","DOIUrl":"10.1016/j.ijheh.2024.114470","url":null,"abstract":"<div><div>Previous studies have suggested that metal/metalloid (hereafter referred to as metal) exposure may influence placental growth by affecting gene expression in the placenta. However, no epidemiological studies have been conducted to validate the relationships between metals exposure, placental gene expression, and placental growth at the population level. This study aims to investigate these relationships based on Hangzhou birth cohort study II (HBCS-II). Totally, 1025 participants were derived from HBCS-II. Thirteen metals levels in the placenta were measured using inductively coupled plasma mass spectrometry. Placental growth characteristics were assessed, including placental weight, chorionic disc area, placental eccentricity, and distance from cord insertion site to the nearest edge of placenta (DCIEP). The relationships between metals exposure and placental growth characteristics were examined using the elastic net model combined unpenalized linear regression model. Placental gene expression levels were analyzed through RNA sequencing and real-time polymerase chain reaction (RT-qPCR), and mediation analysis was conducted to investigate whether placental gene expression could mediate the relationship between metal exposure and placental growth. Notably, the results showed that a unite increase in Ln-transformed cadmium (Cd) levels was associated with a reduction of 16.4 g [95% confidence interval (CI): 31.2, −1.5] in placental weight, 13.9 cm<sup>2</sup> (95%CI: 20.0, −7.8) in chorionic disc area, and 0.3 cm (95%CI: 0.55, −0.06) in DCIEP. Through RNA sequencing followed by validation, significant associations were observed between placental Cd level and increased expression of placental genes, including <em>TNFAIP2</em>, <em>OLAH</em>, <em>FLT4</em>, <em>SH3PXD2A</em>, <em>LIMCH1</em>, <em>BCL6</em>, <em>SLCO2A1</em>, and <em>CPSF1</em>. Additionally, increased placental <em>TNFAIP2</em>, <em>OLAH</em>, <em>FLT4</em>, <em>SH3PXD2A</em> and <em>LIMCH1</em> expression was linked to reduced placental weight. Moreover, <em>SH3PXD2A</em> was associated with decreased chorionic disc area. Mediation analysis showed that placental Cd level was associated with a 12.0 g (95%CI: 23.8, −2.7) decrease in placental weight mediated through the upregulation of <em>FTL4</em> gene expression. The study provides evidence of the association between placental Cd exposure and decreased placental weight, and the <em>FLT4</em> gene may play a mediating role in this relationship. Future experiment studies should be performed to validate the results.</div></div>","PeriodicalId":13994,"journal":{"name":"International journal of hygiene and environmental health","volume":"263 ","pages":"Article 114470"},"PeriodicalIF":4.5,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142335205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26DOI: 10.1016/j.ijheh.2024.114464
Chloe Friedman , Sierra Niemiec , Dana Dabelea , Katerina Kechris , Ivana V. Yang , John L. Adgate , Deborah H. Glueck , Sheena E. Martenies , Sheryl Magzamen , Anne P. Starling
Background/objectives
Prenatal exposure to ambient air pollution is associated with adverse cardiometabolic outcomes in childhood. We previously observed that prenatal black carbon (BC) was inversely associated with adiponectin, a hormone secreted by adipocytes, in early childhood. Changes to DNA methylation have been proposed as a potential mediator linking in utero exposures to lasting health impacts.
Methods
Among 532 mother-child pairs enrolled in the Colorado-based Healthy Start study, we performed an epigenome-wide association study of the relationship between prenatal exposure to a component of air pollution, BC, and DNA methylation in cord blood. Average pregnancy ambient BC was estimated at the mother's residence using a spatiotemporal prediction model. DNA methylation was measured using the Illumina 450K array. We used multiple linear regression to estimate associations between prenatal ambient BC and 429,246 cysteine-phosphate-guanine sites (CpGs), adjusting for potential confounders. We identified differentially methylated regions (DMRs) using DMRff and ENmix-combp. In a subset of participants (n = 243), we investigated DNA methylation as a potential mediator of the association between prenatal ambient BC and lower adiponectin in childhood.
Results
We identified 44 CpGs associated with average prenatal ambient BC after correcting for multiple testing. Several genes annotated to the top CpGs had reported functions in the immune system. There were 24 DMRs identified by both DMRff and ENmix-combp. One CpG (cg01123250), located on chromosome 2 and annotated to the UNC80 gene, was found to mediate approximately 20% of the effect of prenatal BC on childhood adiponectin, though the confidence interval was wide (95% CI: 3, 84).
Conclusions
Prenatal BC was associated with DNA methylation in cord blood at several sites and regions in the genome. DNA methylation may partially mediate associations between prenatal BC and childhood cardiometabolic outcomes.
背景/目的产前暴露于环境空气污染与儿童期不良的心脏代谢结果有关。我们以前曾观察到，产前黑碳（BC）与儿童早期的脂肪细胞分泌的一种激素--脂肪连素成反比。方法在科罗拉多州健康起步研究中登记的 532 对母子中，我们对产前暴露于空气污染成分 BC 与脐带血中 DNA 甲基化之间的关系进行了一项全表观基因组关联研究。利用时空预测模型估算了母亲居住地的平均孕期环境 BC 值。DNA 甲基化使用 Illumina 450K 阵列进行测量。我们使用多元线性回归估计了产前环境 BC 与 429,246 个半胱氨酸-磷酸鸟嘌呤位点（CpGs）之间的关联，并对潜在的混杂因素进行了调整。我们使用 DMRff 和 ENmix-combp 确定了差异甲基化区域（DMRs）。在一部分参与者（n = 243）中，我们研究了 DNA 甲基化作为产前环境 BC 与儿童期较低的脂肪连蛋白之间关联的潜在中介因素的作用。据报道，注释到最高CpGs的几个基因具有免疫系统功能。通过 DMRff 和 ENmix-combp 发现了 24 个 DMRs。其中一个CpG（cg01123250）位于2号染色体，注释为UNC80基因，被发现介导了产前BC对儿童脂肪连素影响的约20%，但置信区间较宽（95% CI：3，84）。DNA甲基化可能部分介导了产前碱性磷酸酶与儿童心脏代谢结果之间的关系。
{"title":"Prenatal black carbon exposure and DNA methylation in umbilical cord blood","authors":"Chloe Friedman , Sierra Niemiec , Dana Dabelea , Katerina Kechris , Ivana V. Yang , John L. Adgate , Deborah H. Glueck , Sheena E. Martenies , Sheryl Magzamen , Anne P. Starling","doi":"10.1016/j.ijheh.2024.114464","DOIUrl":"10.1016/j.ijheh.2024.114464","url":null,"abstract":"<div><h3>Background/objectives</h3><div>Prenatal exposure to ambient air pollution is associated with adverse cardiometabolic outcomes in childhood. We previously observed that prenatal black carbon (BC) was inversely associated with adiponectin, a hormone secreted by adipocytes, in early childhood. Changes to DNA methylation have been proposed as a potential mediator linking <em>in utero</em> exposures to lasting health impacts.</div></div><div><h3>Methods</h3><div>Among 532 mother-child pairs enrolled in the Colorado-based Healthy Start study, we performed an epigenome-wide association study of the relationship between prenatal exposure to a component of air pollution, BC, and DNA methylation in cord blood. Average pregnancy ambient BC was estimated at the mother's residence using a spatiotemporal prediction model. DNA methylation was measured using the Illumina 450K array. We used multiple linear regression to estimate associations between prenatal ambient BC and 429,246 cysteine-phosphate-guanine sites (CpGs), adjusting for potential confounders. We identified differentially methylated regions (DMRs) using DMRff and ENmix-combp. In a subset of participants (n = 243), we investigated DNA methylation as a potential mediator of the association between prenatal ambient BC and lower adiponectin in childhood.</div></div><div><h3>Results</h3><div>We identified 44 CpGs associated with average prenatal ambient BC after correcting for multiple testing. Several genes annotated to the top CpGs had reported functions in the immune system. There were 24 DMRs identified by both DMRff and ENmix-combp. One CpG (cg01123250), located on chromosome 2 and annotated to the <em>UNC80</em> gene, was found to mediate approximately 20% of the effect of prenatal BC on childhood adiponectin, though the confidence interval was wide (95% CI: 3, 84).</div></div><div><h3>Conclusions</h3><div>Prenatal BC was associated with DNA methylation in cord blood at several sites and regions in the genome. DNA methylation may partially mediate associations between prenatal BC and childhood cardiometabolic outcomes.</div></div>","PeriodicalId":13994,"journal":{"name":"International journal of hygiene and environmental health","volume":"263 ","pages":"Article 114464"},"PeriodicalIF":4.5,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26DOI: 10.1016/j.ijheh.2024.114468
Jie He, Lauren M. Smith, Abas Shkembi, Richard L. Neitzel
Objectives
This study assessed the relationship between occupational noise exposure and the incidence of workplace fatal injury (FI) and nonfatal injury (NFI) in the United States from 2006 to 2020. It also examined whether distinct occupational and industrial clusters based on noise exposure characteristics demonstrated varying risks for FI and NFI.
Methods
An ecological study design was utilized, employing data from the U.S. Bureau of Labor Statistics for FI and NFI and demographic data, the U.S. Census Bureau for occupation/industry classification code lists, and the U.S./Canada Occupational Noise Job Exposure Matrix for noise measurements. We examined four noise metrics as predictors of FI and NFI rates: mean Time-Weighted Average (TWA), maximum TWA, standard deviation of TWA, and percentage of work shifts exceeding 85 or 90 dBA for 619 occupation-years and 591 industry-years. K-means clustering was used to identify clusters of noise exposure characteristics. Mixed-effects negative binomial regression examined the relationship between the noise characteristics and FI/NFI rates separately for occupation and industry.
Results
Among occupations, we found significant associations between increased FI rates and higher mean TWA (IRR: 1.06, 95% CI: 1.01–1.12) and maximum TWA (IRR: 1.10, 95% CI: 1.07–1.14), as well as TWA exceedance (IRR: 1.04, 95% CI: 1.01–1.07). Increased rates of NFI were found to be significantly associated with maximum TWA (IRR: 1.06, 95% CI: 1.04–1.09) and TWA exceedance (IRR: 1.03, 95% CI: 1.01–1.05). In addition, occupations with both higher exposure variability (IRR with FI rate: 1.49, 95% CI: 1.23–1.80; IRR with NFI rate: 1.40, 95% CI: 1.14–1.73) and higher level of sustained exposure (IRR with FI rate: 1.27, 95% CI: 1.12–1.44; IRR with NFI rate: 1.21, 95% CI: 1.05–1.39) were associated with higher rates of FI and NFI compared to occupations with low noise exposure. Among industries, significant associations between increased NFI rates and higher mean TWA (IRR: 1.05, 95% CI: 1.02–1.08) and maximum TWA (IRR: 1.06, 95% CI: 1.04–1.08) were observed. Unlike the occupation-specific analysis, industries with higher exposure variability and higher sustained exposures did not display significantly higher FI/NFI rates compared to industries with low exposure.
Conclusions
The results suggest that occupational noise exposure may be an independent risk factor for workplace FIs/NFIs, particularly for workplaces with highly variable noise exposures. The study highlights the importance of comprehensive occupational noise assessments.
目标本研究评估了 2006 年至 2020 年美国职业噪声暴露与工作场所致命伤害 (FI) 和非致命伤害 (NFI) 发生率之间的关系。研究采用了生态学研究设计，使用了美国劳工统计局的 FI 和 NFI 数据以及人口统计数据、美国人口普查局的职业/行业分类代码表和美国/加拿大职业噪声工作暴露矩阵的噪声测量数据。我们研究了预测 FI 和 NFI 发生率的四个噪声指标：619 个职业年和 591 个行业年的平均加权时间平均值 (TWA)、最大 TWA、TWA 标准偏差以及超过 85 或 90 dBA 的工作班次百分比。K-means 聚类法用于识别噪声暴露特征的聚类。结果在各种职业中，我们发现 FI 率增加与平均 TWA（IRR：1.06，95% CI：1.01-1.12）和最大 TWA（IRR：1.10，95% CI：1.07-1.14）以及 TWA 超标（IRR：1.04，95% CI：1.01-1.07）之间存在显著关联。NFI 的增加与最大 TWA（IRR：1.06，95% CI：1.04-1.09）和 TWA 超标（IRR：1.03，95% CI：1.01-1.05）显著相关。此外，暴露变异性较高的职业（含 FI 率的 IRR：1.49，95% CI：1.01-1.051.49, 95% CI: 1.23-1.80; IRR with NFI rate：1.40，95% CI：1.14-1.73）和持续暴露水平较高（带 FI 比率的 IRR：1.27，95% CI：1.14-1.73）的职业：1.27, 95% CI: 1.12-1.44; IRR with NFI rate：与低噪声暴露的职业相比，较高的 FI 和 NFI 率与较高的持续暴露水平有关（IRR 与 FI 率：1.27，95% CI：1.12-1.44；IRR 与 NFI 率：1.21，95% CI：1.05-1.39）。在各行业中，观察到 NFI 率增加与较高的平均 TWA（IRR：1.05，95% CI：1.02-1.08）和最大 TWA（IRR：1.06，95% CI：1.04-1.08）之间存在明显关联。结果表明，职业噪声暴露可能是工作场所 FIs/NFIs 的一个独立风险因素，尤其是在噪声暴露高度可变的工作场所。这项研究强调了全面职业噪声评估的重要性。
{"title":"Evaluating the impact of occupational noise exposure on workplace fatal and nonfatal injuries in the U.S. (2006–2020)","authors":"Jie He, Lauren M. Smith, Abas Shkembi, Richard L. Neitzel","doi":"10.1016/j.ijheh.2024.114468","DOIUrl":"10.1016/j.ijheh.2024.114468","url":null,"abstract":"<div><h3>Objectives</h3><div>This study assessed the relationship between occupational noise exposure and the incidence of workplace fatal injury (FI) and nonfatal injury (NFI) in the United States from 2006 to 2020. It also examined whether distinct occupational and industrial clusters based on noise exposure characteristics demonstrated varying risks for FI and NFI.</div></div><div><h3>Methods</h3><div>An ecological study design was utilized, employing data from the U.S. Bureau of Labor Statistics for FI and NFI and demographic data, the U.S. Census Bureau for occupation/industry classification code lists, and the U.S./Canada Occupational Noise Job Exposure Matrix for noise measurements. We examined four noise metrics as predictors of FI and NFI rates: mean Time-Weighted Average (TWA), maximum TWA, standard deviation of TWA, and percentage of work shifts exceeding 85 or 90 dBA for 619 occupation-years and 591 industry-years. K-means clustering was used to identify clusters of noise exposure characteristics. Mixed-effects negative binomial regression examined the relationship between the noise characteristics and FI/NFI rates separately for occupation and industry.</div></div><div><h3>Results</h3><div>Among occupations, we found significant associations between increased FI rates and higher mean TWA (IRR: 1.06, 95% CI: 1.01–1.12) and maximum TWA (IRR: 1.10, 95% CI: 1.07–1.14), as well as TWA exceedance (IRR: 1.04, 95% CI: 1.01–1.07). Increased rates of NFI were found to be significantly associated with maximum TWA (IRR: 1.06, 95% CI: 1.04–1.09) and TWA exceedance (IRR: 1.03, 95% CI: 1.01–1.05). In addition, occupations with both higher exposure variability (IRR with FI rate: 1.49, 95% CI: 1.23–1.80; IRR with NFI rate: 1.40, 95% CI: 1.14–1.73) and higher level of sustained exposure (IRR with FI rate: 1.27, 95% CI: 1.12–1.44; IRR with NFI rate: 1.21, 95% CI: 1.05–1.39) were associated with higher rates of FI and NFI compared to occupations with low noise exposure. Among industries, significant associations between increased NFI rates and higher mean TWA (IRR: 1.05, 95% CI: 1.02–1.08) and maximum TWA (IRR: 1.06, 95% CI: 1.04–1.08) were observed. Unlike the occupation-specific analysis, industries with higher exposure variability and higher sustained exposures did not display significantly higher FI/NFI rates compared to industries with low exposure.</div></div><div><h3>Conclusions</h3><div>The results suggest that occupational noise exposure may be an independent risk factor for workplace FIs/NFIs, particularly for workplaces with highly variable noise exposures. The study highlights the importance of comprehensive occupational noise assessments.</div></div>","PeriodicalId":13994,"journal":{"name":"International journal of hygiene and environmental health","volume":"263 ","pages":"Article 114468"},"PeriodicalIF":4.5,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26DOI: 10.1016/j.ijheh.2024.114463
Win Wah , Asmare Gelaw , Deborah C. Glass , Malcolm R. Sim , Ryan F. Hoy , Janneke Berecki-Gisolf , Karen Walker-Bone
Background
Wildfire smoke contains numerous hazardous air pollutants which pose serious health risks to humans. Despite this, there has been a limited focus on the assessment of the acute physiological and longer-term respiratory effects of wildfire exposure on firefighters and other emergency workers. Therefore, we undertook a systematic review of the evidence about the respiratory impacts of occupational wildfire smoke exposure among wildfire fighters (WFF).
Methods
Eligible studies from Medline, Embase and Scopus databases were included if they described the relationship between wildfire exposure and respiratory function, symptoms, measures and diseases amongst emergency personnel or firefighters who had responded to wildfires.
Results
Twenty-six articles met the inclusion criteria. 24 out of 26 (22 out of 23 moderate/high quality) studies provided evidence of adverse respiratory effects, including reduced lung function, increased airway dysfunction and airway inflammation, upper and lower respiratory tract symptoms and increased asthma incidence related to wildfires or prescribed burns exposure among WFF and police responders. Fourteen out of 19 studies showed statistically significant declines in spirometry measures of lung function (mostly short-term studies). Two studies using complex lung function tests showed a significant effect on peripheral airway function.
Discussion
This review found a convincing body of evidence that occupational exposure to wildfires or prescribed burns has both acute and possibly longer-term respiratory effects among WFFs and some other emergency personnel. Given that these events are increasing, more needs to be done to identify those most at risk and mitigate these risks.
{"title":"Systematic review of impacts of occupational exposure to wildfire smoke on respiratory function, symptoms, measures and diseases","authors":"Win Wah , Asmare Gelaw , Deborah C. Glass , Malcolm R. Sim , Ryan F. Hoy , Janneke Berecki-Gisolf , Karen Walker-Bone","doi":"10.1016/j.ijheh.2024.114463","DOIUrl":"10.1016/j.ijheh.2024.114463","url":null,"abstract":"<div><h3>Background</h3><div>Wildfire smoke contains numerous hazardous air pollutants which pose serious health risks to humans. Despite this, there has been a limited focus on the assessment of the acute physiological and longer-term respiratory effects of wildfire exposure on firefighters and other emergency workers. Therefore, we undertook a systematic review of the evidence about the respiratory impacts of occupational wildfire smoke exposure among wildfire fighters (WFF).</div></div><div><h3>Methods</h3><div>Eligible studies from Medline, Embase and Scopus databases were included if they described the relationship between wildfire exposure and respiratory function, symptoms, measures and diseases amongst emergency personnel or firefighters who had responded to wildfires.</div></div><div><h3>Results</h3><div>Twenty-six articles met the inclusion criteria. 24 out of 26 (22 out of 23 moderate/high quality) studies provided evidence of adverse respiratory effects, including reduced lung function, increased airway dysfunction and airway inflammation, upper and lower respiratory tract symptoms and increased asthma incidence related to wildfires or prescribed burns exposure among WFF and police responders. Fourteen out of 19 studies showed statistically significant declines in spirometry measures of lung function (mostly short-term studies). Two studies using complex lung function tests showed a significant effect on peripheral airway function.</div></div><div><h3>Discussion</h3><div>This review found a convincing body of evidence that occupational exposure to wildfires or prescribed burns has both acute and possibly longer-term respiratory effects among WFFs and some other emergency personnel. Given that these events are increasing, more needs to be done to identify those most at risk and mitigate these risks.</div></div>","PeriodicalId":13994,"journal":{"name":"International journal of hygiene and environmental health","volume":"263 ","pages":"Article 114463"},"PeriodicalIF":4.5,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-25DOI: 10.1016/j.ijheh.2024.114469
Trisha Saha , M. Corinaud J. Gbemavo , Linda Booij , Tye E. Arbuckle , Jillian Ashley-Martin , Mandy Fisher , Gina Muckle , Bruce Lanphear , Elizabeth Asztalos , Jean Séguin , Maryse F. Bouchard
Exposure to per- and polyfluoroalkyl substances (PFAS) is ubiquitous and may be associated with neurodevelopmental toxicity. However, epidemiological studies report mixed results on the risks of gestational PFAS exposure for children's neurobehavioral impairment. We aimed to examine the associations between prenatal PFAS exposure and children's neurobehavioral and social problems.
We measured plasma concentrations of perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), and perfluorohexane sulphonate (PFHxS) in first-trimester blood from 757 women from the Canadian Maternal-Infant Research on Environmental Chemicals (MIREC) study. Children were assessed at 3–4 years with the Behavior Assessment System for Children-2 (BASC-2) and the Social Responsiveness Scale-2 (SRS-2) (n = 756 and 496, respectively). We used multivariable linear regression to examine associations between individual and summed log2-transformed PFAS and scores on these assessments. Effect modification by sex was evaluated through interaction terms and stratified analyses.
In the sample combining both sexes, a doubling of maternal PFOA was significantly associated with lower T-scores on the following SRS-2 scales: Social Motivation, DSM-Social Communication, and SRS Total score (B ranging from -1.08 to -0.78), suggesting lesser impairments with higher exposure. In sex-stratified analysis, PFOA was related to significantly lower T-scores in boys for these BASC-2 scales: Behavioral Symptoms Index, Externalizing Problems, Aggression, and Hyperactivity (B ranging from -1.32 to -1.03). In girls, however, PFAS were significantly associated more problem behaviors, but most associations were small and the CIs included the null, with the exception of PFOA being significantly associated with higher T-scores for the BASC-2Anxiety scale (B = 1.84, 95% CI: 0.36, 3.32).
In conclusion, we did not observe strong associations between prenatal exposure to the PFAS evaluated and children's neurobehavioral and social development in this population with low exposure levels. The results show mixed findings, depending on children's sex, neurodevelopmental outcome, and specific PFAS.
{"title":"Prenatal exposure to PFAS and the association with neurobehavioral and social development during childhood","authors":"Trisha Saha , M. Corinaud J. Gbemavo , Linda Booij , Tye E. Arbuckle , Jillian Ashley-Martin , Mandy Fisher , Gina Muckle , Bruce Lanphear , Elizabeth Asztalos , Jean Séguin , Maryse F. Bouchard","doi":"10.1016/j.ijheh.2024.114469","DOIUrl":"10.1016/j.ijheh.2024.114469","url":null,"abstract":"<div><div>Exposure to per- and polyfluoroalkyl substances (PFAS) is ubiquitous and may be associated with neurodevelopmental toxicity. However, epidemiological studies report mixed results on the risks of gestational PFAS exposure for children's neurobehavioral impairment. We aimed to examine the associations between prenatal PFAS exposure and children's neurobehavioral and social problems.</div><div>We measured plasma concentrations of perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), and perfluorohexane sulphonate (PFHxS) in first-trimester blood from 757 women from the Canadian Maternal-Infant Research on Environmental Chemicals (MIREC) study. Children were assessed at 3–4 years with the Behavior Assessment System for Children-2 (BASC-2) and the Social Responsiveness Scale-2 (SRS-2) (n = 756 and 496, respectively). We used multivariable linear regression to examine associations between individual and summed log<sub>2</sub>-transformed PFAS and scores on these assessments. Effect modification by sex was evaluated through interaction terms and stratified analyses.</div><div>In the sample combining both sexes, a doubling of maternal PFOA was significantly associated with lower T-scores on the following SRS-2 scales: Social Motivation, DSM-Social Communication, and SRS Total score (B ranging from -1.08 to -0.78), suggesting lesser impairments with higher exposure. In sex-stratified analysis, PFOA was related to significantly lower T-scores in boys for these BASC-2 scales: Behavioral Symptoms Index, Externalizing Problems, Aggression, and Hyperactivity (B ranging from -1.32 to -1.03). In girls, however, PFAS were significantly associated more problem behaviors, but most associations were small and the CIs included the null, with the exception of PFOA being significantly associated with higher T-scores for the BASC-2Anxiety scale (B = 1.84, 95% CI: 0.36, 3.32).</div><div>In conclusion, we did not observe strong associations between prenatal exposure to the PFAS evaluated and children's neurobehavioral and social development in this population with low exposure levels. The results show mixed findings, depending on children's sex, neurodevelopmental outcome, and specific PFAS.</div></div>","PeriodicalId":13994,"journal":{"name":"International journal of hygiene and environmental health","volume":"263 ","pages":"Article 114469"},"PeriodicalIF":4.5,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142319636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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