Pulmonary toxicity associated with occupational and environmental exposure to pesticides and herbicides

Abstract

Purpose of review Critical review on the notion that exposure to pesticides and herbicides lead to adverse effects in pulmonary health. Recent findings The lung effects of several chemical classes of pesticides and herbicides is biologically plausible. However, the studies that describe the association between exposure and toxic lung effects have numerous limitations. Critical evaluation of the studies that are performed shows that assessment of occupational or environmental exposure to pesticides and herbicides is cumbersome. Moreover, the health effects are not always clearly established due to the use of questionnaires and self-reported data instead of lung function measurements or diagnostic work-up by physicians. Future studies should preferably better characterize the exposure. Genetic phenotyping should be included to understand and strengthen possible (individual) associations between exposure and health outcome. It should be realized that combined exposure to multiple environmental chemicals may lead to different health effects than exposure to individual chemicals. Summary The relation between exposure to pesticides and herbicides and lung toxicity is less clear than generally assumed. Adverse lung effects seem multifactorial and needs further research. Preventive measures remain key.

Current status of pesticide effects on environment, human health and it’s eco-friendly management as bioremediation: A comprehensive review

“…Several epidemiological and molecular research highlighted a close association between persistent pesticides exposure and increased risk of diseases such as neurodegenerative disorders, endocrine disruptors, respiratory complications, reproductive disorders, and birth defects ( García et al, 2017 ; Larsen et al, 2017 ; Addissie et al, 2020 ; Bast et al, 2021 ; Bhadauriya et al, 2021 ; Witczak et al, 2021 ; Gea et al, 2022 ; Iteire et al, 2022 ). In addition, the carcinogenic, teratogenic, and mutagenic nature of these compounds are also believed to be a contributing source of cancer development in the human population.…”

Glyphosate: Hepatotoxicity, Nephrotoxicity, Hemotoxicity, Carcinogenicity, and Clinical Cases of Endocrine, Reproductive, Cardiovascular, and Pulmonary System Intoxication

“…Lung diseases refer to pathologies of airways, air sacs, and vascular and neuromuscular elements of respiration, leading to airway obstruction, lung compliance, and the blockage of gas exchange. Major causative factors of respiratory diseases include autoimmune risks, allergens, infections, sepsis, cold, burns, smoking, air pollution, heavy metals, coal dust, asbestos, combat gases, and persistent exposition to agrochemicals. − …”

“…Regarding occupational disorders, asthma, chronic bronchitis, chronic obstructive pulmonary disease (COPD), and pneumonia are most frequent among agricultural workers . Herbicide exposition-related lung disease case studies mentioned asthma, COPD, acute fibrinous and organizing pneumonia, pulmonary fibrosis, and lung cancer, as reviewed elsewhere , (Figure ). Mechanisms of agrochemical-caused respiratory pathophysiology associated with oxidative stress, inhibition of the parasympathetic system followed by airway hyperactivity, immunological alterations, including macrophage infiltration and eosinophil abscesses, and allergic response. − The risk of agricultural airborne exposure to GLP involves inhaling the GLP containing eroded sediments and dust.…”

Modeling the Effects of Cypermethrin Toxicity on Ovalbumin-Induced Allergic Pneumonitis Rats: Macrophage Phenotype Differentiation and p38/STAT6 Signaling Are Candidate Targets of Pirfenidone Treatment

“…Chronic asthma patients are susceptible individuals whose allergy could be worsened by insecticide exposure due to immunological shifts and alterations [ 11 ]. Therefore, the aim of the study was, first, to investigate the possible exacerbation of severe allergic lung inflammation and the possible induction of steroid resistance, due to oral CYP exposure, in concurrently existing asthma in albino rats.…”