Background: Exhaled nitric oxide is a marker of airway inflammation. Air pollution induces airway inflammation and oxidative stress. Little is known about the impact of air pollution on exhaled nitric oxide in young infants.
Methods: The Breathing for Life Trial recruited pregnant women with asthma into a randomised controlled trial comparing usual clinical care versus inflammometry-guided asthma management in pregnancy. Four hundred fifty-seven infants from the Breathing for Life Trial birth cohort were assessed at six weeks of age. Exhaled nitric oxide was measured in unsedated, sleeping infants. Its association with local mean 24-h and mean seven-day concentrations of ozone, nitric oxide, nitrogen dioxide, carbon monoxide, sulfur dioxide, ammonia, particulate matter less than 10 μm (PM10) and less than 2.5 μm (PM2.5) in diameter was investigated. The air pollutant data were sourced from local monitoring sites of the New South Wales Air Quality Monitoring Network. The association was assessed using a 'least absolute shrinkage and selection operator' (LASSO) approach, multivariable regression and Spearman's rank correlation.
Results: A seasonal variation was evident with higher median exhaled nitric oxide levels (13.6 ppb) in warmer months and lower median exhaled nitric oxide levels (11.0 ppb) in cooler months, P = 0.008. LASSO identified positive associations for exhaled nitric oxide with 24-h mean ammonia, seven-day mean ammonia, seven-day mean PM10, seven-day mean PM2.5, and seven-day mean ozone; and negative associations for eNO with seven-day mean carbon monoxide, 24-h mean nitric oxide and 24-h mean sulfur dioxide, with an R-square of 0.25 for the penalized coefficients. These coefficients selected by LASSO (and confounders) were entered in multivariable regression. The achieved R-square was 0.27.
Conclusion: In this cohort of young infants of asthmatic mothers, exhaled nitric oxide showed seasonal variation and an association with local air pollution concentrations.
Background: Acute bronchiolitis and air pollution are both risk factor of pediatric asthma. This study aimed to assess subsequent exposure to air pollutants related to the inception of preschool asthma in infants with acute bronchiolitis. This study aimed to assess subsequent exposure to air pollutants related to the inception of preschool asthma in infants with acute bronchiolitis.
Methods: A nested case-control retrospective study was performed at the Kaohsiung Medical University Hospital systems between 2009 and 2019. The average concentration of PM10, PM2.5, SO2, NO, NO2, and NOX was collected for three, six, and twelve months after the first infected episode. Adjusted regression models were employed to evaluate the association between asthma and air pollution exposure after bronchiolitis.
Results: Two thousand six hundred thirty-seven children with acute bronchiolitis were included. Exposure to PM10, PM2.5, SO2, NO, NO2, and NOX in the three, six, and twelve months following an episode of bronchiolitis was found to significantly increase the risk of preschool asthma in infants with a history of bronchiolitis.(OR, 95%CI: PM10 = 1.517-1.559, 1.354-1.744; PM2.5 = 2.510-2.603, 2.148-3.061; SO2 = 1.970-2.040, 1.724-2.342; ; NO = 1.915-1.950, 1.647-2.272; NO2 = 1.915-1.950, 1.647-2.272; NOX = 1.752-1.970, 1.508-2.252) In a sensitive analysis of hospitalized infants, only PM10, PM2.5, SO2, and NO were found to have significant effects during all time periods. (OR, 95%CI: PM10 = 1.613-1.650, 1.240-2.140; PM2.5 = 2.208-2.286, 1.568-3.061; SO2 = 1.679-1.622, 1.197-2.292; NO = 1.525-1.557, 1.094-2.181) CONCLUSION: The presence of ambient PM10, PM2.5, SO2 and NO in the three, six, and twelve months following an episode of acute bronchiolitis has been linked to the development of preschool asthma in infants with a history of acute bronchiolitis.
Background: Respirable crystalline silica (RCS) is associated with the development of lung cancer. However, there is uncertainty around the exposure threshold at which exposure to RCS may pose a clear risk for the development of lung cancer. The objective of this study was to review the cut-off points at which the risk of mortality or incidence of lung cancer due to occupational exposure to RCS becomes evident through a systematic review.
Methods: We conducted a search in PubMed, including cohort and case-control studies which assessed various categories of RCS exposure. A search was also conducted on the webpages of institutional organizations. A qualitative data synthesis was performed.
Results: Twenty studies were included. Studies that assessed lung cancer mortality and incidence displayed wide variability both in RCS exposure categories and related risks. Although most studies found no significant association for RCS exposure categories, it appears to be a low risk of lung cancer for mean concentrations of less than 0.07mg/m3. Regulatory agencies set annual RCS exposure limits ranging from 0.025mg/m3 through 0.1mg/m3.
Conclusions: There is a wide degree of heterogeneity in RCS exposure categories, with most studies observing no significant risk of lung cancer for the lowest exposure categories. Cut-off points differ between agencies but are nonetheless very similar and do not exceed 0.1mg/m3.
Background: Phthalate esters (PAEs) are known to have hormone-like properties, and there is a growing trend of children expressing a gender identity different from assigned sex. However, there has been limited research in the potential links between PAEs exposure and gender identity.
Methods: A total of 571 children (278 boys) completed the follow-up from Oct 2017 to Oct 2020 in Childhood Blood Pressure and Environmental Factors (CBPEF) cohort in Xiamen, China. Urinary PAE metabolites were measured at three time of visits using ultraperformance liquid chromatography-tandem mass spectrometry. The Children's Sex Role Inventory scale was used to assess gender identity (masculinity, femininity, androgyny and undifferentiated), and Tanner definition was used to define puberty timing. Generalized linear models and log-binomial regression were used to assess the relationships between PAEs exposure, gender trait scores and gender identity.
Results: Overall, the concentration of most PAEs in more than 90% of participants was above the limit of detection values. In visit 1, there were 10.1% boys with femininity and 11.3% girls with masculinity; while these figures increased to 10.8% and 12.3% during follow-up, respectively. Early puberty onset accounted for 24.8% and 25.6% among boys and girls. Long-term exposure to mono-2-ethylhexyl phthalate (MEHP) (β = 1.20, 95%CI = 0.13, 2.28), mono-2-ethyl-5-hydroxyhexyl phthalate (MEHHP) (β = 1.25, 95%CI = 0.22, 2.28) and mono-2-ethyl-5-oxohexyl phthalate (MEOHP) (β = 1.40, 95%CI = 0.24, 2.56) was associated with the increased differences of femininity trait scores in boys who enter puberty earlier, prolonged exposure to di(2-ethylhexyl) phthalate (DEHP) might also have such a positive impact (β = 1.38, 95%CI = 0.36, 2.41). For gender identity, persistent exposure to low molecular weight phthalates (LMWP) was negatively associated with undifferentiated type among boys entering puberty earlier (RR = 0.18, 95%CI = 0.05, 0.75, P < 0.05), and most of the PAE metabolites exposures showed risk ratios > 1 for their femininity.
Conclusion: Long-term exposure to PAEs increase the femininity trait scores in boys with early onset of puberty. Although the mechanisms remain to be determined, environmental pollution might have subtle, yet measurable effects on childhood gender identity. Reducing these chemicals exposure has important public implications on gender development.
Background: Early life exposure to lead, mercury, polychlorinated biphenyls (PCBs), polybromide diphenyl ethers (PBDEs), organophosphate pesticides (OPPs), and phthalates have been associated with lowered IQ in children. In some studies, these neurotoxicants impact males and females differently. We aimed to examine the sex-specific effects of exposure to developmental neurotoxicants on intelligence (IQ) in a systematic review and meta-analysis.
Method: We screened abstracts published in PsychINFO and PubMed before December 31st, 2021, for empirical studies of six neurotoxicants (lead, mercury, PCBs, PBDEs, OPPs, and phthalates) that (1) used an individualized biomarker; (2) measured exposure during the prenatal period or before age six; and (3) provided effect estimates on general, nonverbal, and/or verbal IQ by sex. We assessed each study for risk of bias and evaluated the certainty of the evidence using Navigation Guide. We performed separate random effect meta-analyses by sex and timing of exposure with subgroup analyses by neurotoxicant.
Results: Fifty-one studies were included in the systematic review and 20 in the meta-analysis. Prenatal exposure to developmental neurotoxicants was associated with decreased general and nonverbal IQ in males, especially for lead. No significant effects were found for verbal IQ, or postnatal lead exposure and general IQ. Due to the limited number of studies, we were unable to analyze postnatal effects of any of the other neurotoxicants.
Conclusion: During fetal development, males may be more vulnerable than females to general and nonverbal intellectual deficits from neurotoxic exposures, especially from lead. More research is needed to examine the nuanced sex-specific effects found for postnatal exposure to toxic chemicals.
Background: The need to call out and expose authors for their persistence in improperly using epidemiology has been previously noted. Tsuda et al. have done well to expose Schüz et al.'s arguments/assertions in their recent publication in Environmental Heath. In this Comment, I point out that, also warranting being called out, are the arguments/assertions of Cléro et al. who, in their recent response to an article by Tsuda et al., reiterated the conclusions and recommendations derived from their European project, which were published in Environment International in 2021. Tsuda et al. had critiqued the Cléro et al. 2021 publication in their 2022 review article. However, in their response to it, Cléro et al. deflected by not addressing any of the key points that Tsuda et al. had made in their review regarding the aftermath of the Chernobyl and Fukushima nuclear accidents. In this Comment, I critique Cléro et al.'s inadequate response. Publication of this Comment will help in routing out the improper use of epidemiology in the formulation of public health policy and thereby reduce the influence of misinformation on both science and public policy. My critique of Cléro et al. is not dissimilar from Tsuda et al.'s critique of Schüz et al.: in as much as Schüz et al. should withdraw their work, so should Cléro et al.'s article be retracted.
Main body: The response by Cléro et al. consists of four paragraphs. First was their assertion that the purpose of the SHAMISEN project was to make recommendations based on scientific evidence and that it was not a systematic review of all related articles. I point out that the Cléro et al. recommendations were not based on objective scientific evidence, but on biased studies. In the second paragraph, Cléro et al. reaffirmed the SHAMISEN Consortium report, which claimed that the overdiagnosis observed in non-exposed adults was applicable to children because children are mirrors of adults. However, the authors of that report withheld statements about secondary examinations in Fukushima that provided evidence against overdiagnosis. In the third paragraph, Cléro et al. provided an explanation regarding their disclosure of conflicting interests, which was contrary to professional norms for transparency and thus was unacceptable. Finally, their insistence that the Tsuda et al. study was an ecological study susceptible to "the ecological fallacy" indicated their lack of epidemiological knowledge about ecological studies. Ironically, many of the papers cited by Cléro et al. regarding overdiagnosis were, in fact, ecological studies.
Conclusion: Cléro et al. and the SHAMISEN Consortium should withdraw their recommendation "not to launch a mass thyroid cancer screening after a nuclear accident, but rather to make it available (with appropriate information counselling) to those who request it." Their recommendation is based on biased evidence and would cause conf
Perfluoroalkyl and polyfluoroalkyl substances (PFASs) may have a role in impaired health. However, the data on the association between PFASs and Systemic lupus erythematosus (SLE) have been limited. We designed a population-based case-control study in China and evaluated the association. 100 normal persons (Control) and 100 SLE patients (Case) were obtained from 113 controls and 125 cases according to matching conditions. Serum samples were collected by venipuncture for UHPLC-MRM-MS Analysis to obtain the concentration of five PFASs in participants. Demographic characterization description was performed for the two groups of participants, the PFASs concentration distribution of the two groups was described and compared, then divided into three tiers (< 50th, 50th ~ 75th, > 75th) for subsequent analysis. Conditional logistic regression models were utilized to calculate the odds ratios (ORs) and 95% CIs for SLE. Relationship between changes in the concentration of PFASs and the risk of SLE assessed by restricted cubic spline. As the highest serum levels of the five PFASs tested in this study population, the highest perfluoroundecanoic acid (PFUnA) quartile had a 2.78-fold (95%CI: 1.270, 6.10) compared with the lowest quartile of PFUnA exposure, other types of PFASs also showed high association with SLE as well as PFASs mixture. Additionally, the exposure of PFASs exist a dose-response relationship (ptrend < 0.05). This risk association remained be found after adjusting the covariates in model 1 (adjustment of BMI) and in model 2(adjustment of BMI, smoking, drinking, hypertension and leukocyte). The restricted cubic spline illustrated a gradual increase in the possible risk of SLE with the increasing exposure of PFASs components levels. Our study firstly revealed that PFASs are risk factors for SLE and PFASs exposures are associated with SLE risk in a dose - response manner. Evidence from larger and more adequately powered cohort studies is needed to confirm our results.
Background: Endometrial cancer is the most common gynaecological tumour in developed countries and disease burden is expected to increase over the years. Identifying modifiable risk factors may help developing strategies to reduce the expected increasing incidence of these neoplasms.
Objective: This study evaluates the association between occupational exposure to pesticides and endometrial cancer using data from a recent case-control study in Spain.
Methods: The analyses included data from 174 consecutive incident endometrial cancer cases and 216 hospital controls frequency-matched by age. Data were collected through structured epidemiological questionnaires and exposure to pesticides was assessed using a Spanish job-exposure matrix (MatEmESp).
Results: Overall, 12% of controls and 18% of cases were occupationally exposed to pesticides. We observed a positive association between occupational exposure to pesticides and endometrial cancer (OR = 2.08; 95% CI = 1.13-3.88 compared to non-exposed). In general, exposures that occurred farther in the past were significantly associated with endometrial cancer. Exposure to insecticides, fungicides and herbicides were positively associated with endometrial cancer (OR = 2.08; 95% CI = 1.13-3.88, OR = 4.40; 95% CI = 1.65-13.33, and OR = 5.25; 95% CI = 1.84-17.67, respectively). The agricultural, poultry and livestock activities scenario was associated with endometrial cancer (OR = 4.16; 95% CI = 1.59-12.32), while the cleaning exposure scenario was not (OR = 1.22; 95% CI = 0.55-2.67).
Conclusions: Assessment of occupational exposure to pesticides assessed using a Spanish job-exposure matrix revealed a positive association with endometrial cancer. The elucidation of the role of pesticide compounds on endometrial cancer should shed a light on the aetiology of this tumour.
Background: Research on the effect of pesticide exposure on health has been largely focused on occupational settings. Few reviews have synthesized the associations between dietary pesticide exposure and health outcomes in non-occupationally exposed adults.
Objective: We aim to summarize the evidence regarding dietary pesticide exposure and non-communicable diseases (NCD) in adults, using a systematic review of prospective studies.
Methods: Electronic and manual searches were performed until July 2023. The inclusion criteria were the following: 1) adults aged ≥ 18years, 2) (non)-randomized trials, prospective cohort studies, 3) dietary exposure to pesticides. A bias analysis was carried out using the Nutrition Evidence Systematic Review guidelines based on the Cochrane ROBINS-I.
Results: A total of 52 studies were retrieved and 6 studies that met the above criteria were included. Studies were conducted either in France or in the United States. The studies investigated the risk of cancer (n = 3), diabetes (n = 1), cardiovascular diseases (n = 1), and mortality (n = 1). The quality of the studies varied with overall grades derived from the bias analysis ranging from low to moderate bias. The level of evidence was estimated as low for the risk of cancer while the grading was not assignable for other outcomes, as only one study per outcome was available.
Conclusions: Although further research is warranted to examine more in depth the relationships between low-dose chronic exposure to pesticides through diet and NCD outcomes in non-occupationally-exposed adults, studies suggest a possible role of exposure to dietary pesticide on health. Standardized methodological guidelines should also be proposed to allow for comparison across studies.
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