Association between occupational heat stress and DNA damage in lymphocytes of workers exposed to hot working environments in a steel industry in Southern India

Temperature (Austin). 2019 Jul 22;6(4):346-359. doi: 10.1080/23328940.2019.1632144. eCollection 2019.

Abstract

Occupational heat stress apart from adverse heat-related health consequences also induces DNA damage in workers exposed to high working temperatures. We investigated the association between chronic heat exposures and Micronuclei (MN) frequency in lymphocytes of 120 workers employed in the steel industry. There was a significant increase in the MN-frequency in exposed workers compared to the unexposed workers (X2 = 47.1; p < 0.0001). While exposed workers had higher risk of DNA damage (Adj. OR = 23.3, 95% CI 8.0-70.8) compared to the unexposed workers, among the exposed workers, the odds of DNA damage was much higher for the workers exposed to high-heat levels (Adj. OR = 81.4; 95% CI 21.3-310.1) even after adjusting for confounders. For exposed workers, years of exposure to heat also had a significant association with higher induction of MN (Adj. OR = 29.7; 95% CI 2.8-315.5). Exposures to chronic heat stress is a significant occupational health risk including damages in sub-cellular level, for workers. Developing protective interventions to reduce heat exposures is imperative in the rising temperature scenario to protect millions of workers across the globe.

Keywords: DNA damage; Occupational heat stress; lymphocyte; micronucleus; physiological strain.

Grants and funding

This study was funded by the Government of India Ministry of Science and Technology, Department of Science & Technology (DST) for funding this research (Grant No. DST/ 690 CCP/(NET-2) PR-37/2012(G). The funders had no role in the study design, collection, analysis, and interpretation of the data, writing of the report, or the decision to submit the article for publication. The researchers are independent of the funders;Department of Science and Technology, Government of India [DST/CCP/ (NET-2) PR-37/2012(G)].