Małgorzata Kupczewska-Dobecka, Katarzyna Konieczko, Joanna Jurewicz
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Most studies evaluating the relationship between occupational exposure and the development of allergic respiratory diseases focus on workers involved in ADCA production or its use as a blowing agent in plastics. The objective is to assess the respiratory sensitizing effects of ADCA in humans due to occupational exposure, based on literature data. The presented data confirm that long-term occupational exposure to ADCA can lead to persistent bronchial hyperreactivity symptoms in workers. 1,1'-azodi(formamide) can induce occupational asthma, with initial symptoms including nasal congestion, conjunctivitis, wheezing, and cough. Subsequently, symptoms such as chest tightness, dyspnea, and nocturnal cough attacks may appear, with a latency period of several years observed before symptom onset. In some cases, symptom progression was noted with continued ADCA exposure, while in others, exposure was discontinued after initial symptoms, preventing observation of symptom exacerbation. Prior exposure to allergens, such as working in bakeries, appears to accelerate symptom onset. Improvement in allergy symptoms has been noted during weekend breaks from work. There is no safe concentration identified for ADCA that would not result in adverse health effects for workers. A concentration of 0.036 mg/m<sup>3</sup> is considered the lowest observed adverse effect concentration, causing critical reduction in lung spirometric parameters. 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In Poland, ADCA is manufactured by a company specializing in the production of polyethylene foam bags and laminates used in various industries including home appliances, electronics, construction, furniture, automotive, and sports and leisure. The mechanism of action of ADCA involves thermal decomposition, resulting in nitrogen, carbon monoxide, as well as ammonia and carbon dioxide as the main gaseous decomposition products. These penetrate the polymer matrix, contributing to expansion and foaming properties. Most studies evaluating the relationship between occupational exposure and the development of allergic respiratory diseases focus on workers involved in ADCA production or its use as a blowing agent in plastics. The objective is to assess the respiratory sensitizing effects of ADCA in humans due to occupational exposure, based on literature data. The presented data confirm that long-term occupational exposure to ADCA can lead to persistent bronchial hyperreactivity symptoms in workers. 1,1'-azodi(formamide) can induce occupational asthma, with initial symptoms including nasal congestion, conjunctivitis, wheezing, and cough. Subsequently, symptoms such as chest tightness, dyspnea, and nocturnal cough attacks may appear, with a latency period of several years observed before symptom onset. In some cases, symptom progression was noted with continued ADCA exposure, while in others, exposure was discontinued after initial symptoms, preventing observation of symptom exacerbation. Prior exposure to allergens, such as working in bakeries, appears to accelerate symptom onset. Improvement in allergy symptoms has been noted during weekend breaks from work. There is no safe concentration identified for ADCA that would not result in adverse health effects for workers. A concentration of 0.036 mg/m<sup>3</sup> is considered the lowest observed adverse effect concentration, causing critical reduction in lung spirometric parameters. 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引用次数: 0
摘要
1,1'-偶氮二甲酰胺(ADCA)被广泛用作发泡剂,是一种用于诱导发泡过程的化学物质。在波兰,ADCA 由一家专门生产聚乙烯泡沫袋和层压板的公司制造,这些产品用于家电、电子、建筑、家具、汽车和运动休闲等多个行业。ADCA 的作用机理是热分解,产生氮气、一氧化碳以及氨气和二氧化碳等主要气态分解产物。这些物质渗透到聚合物基体中,产生膨胀和发泡特性。大多数评估职业接触与过敏性呼吸道疾病之间关系的研究都侧重于参与 ADCA 生产或将其用作塑料发泡剂的工人。本研究的目的是根据文献数据,评估职业接触 ADCA 对人体呼吸道的致敏影响。所提供的数据证实,长期接触 ADCA 会导致工人出现持续的支气管高反应症状。1,1'-偶氮二甲酰胺可诱发职业性哮喘,最初的症状包括鼻塞、结膜炎、喘息和咳嗽。随后,可能会出现胸闷、呼吸困难和夜间咳嗽发作等症状,症状出现前会有几年的潜伏期。在一些病例中,持续接触 ADCA 会导致症状加重,而在另一些病例中,最初出现症状后就停止接触 ADCA,因此无法观察到症状加重的情况。之前接触过敏原(如在面包店工作)似乎会加速症状的出现。周末休息时,过敏症状会有所改善。目前尚未确定不会对工人健康造成不良影响的 ADCA 安全浓度。0.036 毫克/立方米的浓度被认为是观察到的最低不良影响浓度,会导致肺部肺活量参数严重下降。Med Pr Work Health Saf.2024;75(5).
[Effect of occupational exposure to ADCA on the incidence of allergic respiratory reactions - a literature review].
1,1'-azodi(formamide) (azodicarbonamide - ADCA) is widely used as a blowing agent, a chemical substance designed to induce foaming processes. In Poland, ADCA is manufactured by a company specializing in the production of polyethylene foam bags and laminates used in various industries including home appliances, electronics, construction, furniture, automotive, and sports and leisure. The mechanism of action of ADCA involves thermal decomposition, resulting in nitrogen, carbon monoxide, as well as ammonia and carbon dioxide as the main gaseous decomposition products. These penetrate the polymer matrix, contributing to expansion and foaming properties. Most studies evaluating the relationship between occupational exposure and the development of allergic respiratory diseases focus on workers involved in ADCA production or its use as a blowing agent in plastics. The objective is to assess the respiratory sensitizing effects of ADCA in humans due to occupational exposure, based on literature data. The presented data confirm that long-term occupational exposure to ADCA can lead to persistent bronchial hyperreactivity symptoms in workers. 1,1'-azodi(formamide) can induce occupational asthma, with initial symptoms including nasal congestion, conjunctivitis, wheezing, and cough. Subsequently, symptoms such as chest tightness, dyspnea, and nocturnal cough attacks may appear, with a latency period of several years observed before symptom onset. In some cases, symptom progression was noted with continued ADCA exposure, while in others, exposure was discontinued after initial symptoms, preventing observation of symptom exacerbation. Prior exposure to allergens, such as working in bakeries, appears to accelerate symptom onset. Improvement in allergy symptoms has been noted during weekend breaks from work. There is no safe concentration identified for ADCA that would not result in adverse health effects for workers. A concentration of 0.036 mg/m3 is considered the lowest observed adverse effect concentration, causing critical reduction in lung spirometric parameters. Med Pr Work Health Saf. 2024;75(5):455-473.