The Impact of Pesticides on Respiratory Health

The Impact of Pesticides on Respiratory Health

hronic respiratory diseases, including asthma and chronic obstructive pulmonary disease (COPD), are a significant global health concern. According to the World Health Organization, these diseases were the leading cause of total world morbidity and the third leading cause of all global deaths in 2008. The prevalence of asthma, in particular, has been on the rise for several decades, affecting approximately 14% of children worldwide.

While viruses, bacteria, and genetic factors have long been recognized as contributors to respiratory diseases, the role of environmental agents, such as pesticides, is still being debated. Pesticides are chemical substances used to control pests in various settings, including agriculture, gardening, and domestic purposes. The general population can be exposed to pesticides through residues in food, water, and the environment.

This article aims to provide an overview of the existing literature on the respiratory effects of environmental exposure to pesticides. By reviewing epidemiological studies published up until 2013, we can gain insights into the potential risks associated with pesticide exposure and respiratory health in both children and adults.

Children: In Utero Pesticide Exposure

Several studies have focused on the association between prenatal exposure to pesticides and respiratory health outcomes in children. In a study conducted in Spain, researchers found that higher levels of dichlorodiphenyldichloroethylene (DDE), a metabolite of the pesticide dichlorodiphenyl trichloroethane (DDT), in cord blood were associated with an increased risk of wheezing at 4 years of age. Another study in the same cohort confirmed the association between DDE concentrations in cord blood and the risk of asthma at 6 years of age.

Similarly, a study in Germany found that children aged 7-10 years with higher levels of DDE in their blood had a significantly higher risk of asthma. However, not all studies have found a consistent association between prenatal pesticide exposure and respiratory health outcomes. Some studies did not find a significant link between exposure to pesticides during pregnancy and respiratory symptoms or diseases in infants.

Children: Post-Natal Pesticide Exposure

Post-natal pesticide exposure in children has also been investigated in several studies. One study conducted in Lebanon found that different types of pesticide exposure among parents, including residential, domestic, and para-occupational exposure, were associated with a higher risk of respiratory diseases in children. Another study in Southern California showed that exposure to herbicides and other pesticides in the first year of life was associated with an increased risk of asthma diagnosed before the age of 5.

Furthermore, a study in the UK found that high levels of maternal occupational exposure to biocides and fungicides after birth increased the likelihood of wheezing and childhood asthma at 7.5 years. The National Health and Nutrition Examination Survey in the USA also found an association between domestic use of pesticides in the kitchen and dining room and respiratory symptoms in children.

Adults: Environmental Pesticide Exposure

While the respiratory effects of occupational pesticide exposure are well-documented, studies on environmental exposure in adults have yielded less conclusive results. One study conducted in the USA among employees exposed to pesticides stored and handled in a health center found a significant association between the duration of employment and bronchitis and sinusitis reported by the subjects. However, the concentrations of pesticides measured in their serum and urine were not associated with any symptoms.

Studies conducted in pesticide application areas in the USA did not find a significant link between respiratory symptoms or asthma attacks and the use of pesticides. Similarly, a study conducted in China among adults living in rural areas found that regular exposure to insecticides and fertilizers was associated with respiratory symptoms but did not establish a clear causal relationship.

Methodological Considerations and Limitations

It is important to note that the studies reviewed here vary in their methodologies and sample sizes, leading to differing results and conclusions. Most studies relied on self-reporting of symptoms, which can introduce biases in the data. Additionally, the nature and intensity of pesticide exposure were often poorly characterized, making it difficult to establish a clear dose-response relationship.

Further research is needed to better understand the potential respiratory risks associated with environmental exposure to pesticides. Future studies should employ more rigorous designs, such as case-control or cohort studies, and utilize more accurate methods of exposure assessment, including environmental measurements and biomarkers. Longitudinal studies tracking exposures over extended periods prior to the onset of respiratory symptoms would provide valuable insights into the temporal relationship between exposure and health outcomes.


In conclusion, the existing literature suggests that environmental exposure to pesticides may have respiratory health implications, particularly in children. Prenatal exposure to certain pesticides has been associated with an increased risk of asthma and wheezing in young children. Post-natal exposure to pesticides, both in utero and during early childhood, has also been linked to respiratory symptoms and diseases. However, the evidence for respiratory risks in adults exposed to pesticides is less conclusive.

While more research is needed to establish clear causal relationships and better understand the mechanisms involved, it is crucial to take precautions and minimize exposure to pesticides, especially among vulnerable populations such as children. Implementing effective interventions to reduce pesticide exposure and promote respiratory health should be a priority to protect the well-being of individuals and communities.

Note: The information provided in this article is for educational purposes only and should not be considered as medical advice. If you have concerns about pesticide exposure or respiratory health, please consult a healthcare professional.


  1. Regulatory (EU) No 528/2012 of the European Parliament and of the Council of 22 May 2012 concerning the making available on the market and use of biocidal products. Official Journal of the European Union 2012; 55: L167.
  2. AFSSET. Exposition de la population générale aux résidus de pesticides en France. Synthèse des données d'utilisation, de contamination des milieux et d'imprégnation de la population. Plan d'action ORP 2006–2008. Maisons-Alfort, AFSSET 2010; p. 354.
  3. INSERM. Paris, Les éditions Inserm, 2013; p. 1001.
  4. Gascon M, Casas M, Morales E, et al. Dichlorodiphenyldichloroethylene, polychlorinated biphenyls, and asthma among children 6 to 12 years of age: a prospective birth cohort study. Environ Health Perspect 2011; 119: 1671-1675.
  5. Zhang Y, Lin X, Zhou T, et al. Association of organochlorine pesticides and polychlorinated biphenyls with asthma in children: a nested case-control study. Environ Res 2020; 184: 109380.
  6. Stieb DM, Chen L, Eshoul M, et al. Ambient air pollution, birth weight and preterm birth: A systematic review and meta-analysis. Environ Res 2012; 117: 100-111.
  7. Guarnieri M, Balmes JR. Outdoor air pollution and asthma. Lancet 2014; 383: 1581-1592.
  8. Gehring U, Wijga AH, Brauer M, et al. Traffic-related air pollution and the development of asthma and allergies during the first 8 years of life. Am J Respir Crit Care Med 2010; 181: 596-603.
  9. Hernández AF, Parrón T, Alarcón R. Pesticides and asthma. Curr Opin Allergy Clin Immunol 2011; 11: 90-96.
  10. Proskocil BJ, Bruun DA, Lorton JK, et al. Neuroimmune mechanisms of pesticide-induced airway hyperreactivity. Environ Health Perspect 2008; 116: 38-44.
  11. Fukuyama T, Tajima H, Uehara Y, et al. Enhancement of allergic skin responses by prior exposure to pesticides in mice. Toxicol Lett 2002; 134: 113-117.
Back to blog