Cumulative Risk Factors in the Urban Environment: Interaction Between Air Pollution and Malnutrition on the Immune Response of Alveolar Macrophages

LEZON C; BOYER P; DELFOSSE VC; TASAT D; KURTZ M; VIALE D

Virtual

Congreso; SETAC Latin America 14th Biennial Meeting; 2021

Society of Environmental Toxicology and Chemistry

General analysis of the urban population health must take into account the interaction of diverse stressors such as air pollution and malnutrition. Air pollution is the largest and most persistent environmental and public health concern in Latin American megacities. These areas are alsocharacterized by socioeconomic gradients that enhance population inequalities, leading to malnutrition and, consequently compromising the body response to noxae. Either as a single risk factor or in combination with other agents, air pollution causes a wide range of acute and chronic respiratory diseases. The respiratory system is the principal target of air pollution where alveolar macrophages (AM) play a key role providing protection against xenobiotics through a variety ofmechanisms including oxygen dependent pathways and proinflammatory cytokine production. Oxidants could lead to a redox imbalance triggering a number of antioxidant mechanisms, of which the Nrf2-Keap1/ARE signal pathway is the most important to date. However, the mechanism linking air pollution exposure and malnutrition still remains unclear. Based on the above, the present studysought to investigate the effects of exposure to ROFA (Residual Oil Fly Ash, a surrogate of urban air pollution) on the lung immune response in rat nutritional growth retardation (NGR) model. Male weanling rats were fed a diet restricted 20% compared to ad libitum intake for 4 weeks in order to achieve NGR. NGR and Control rats were intranasally instilled with either 1mg/kg body weight of ROFA or its vehicle (Phosphate Buffer Solution) and euthanized 24h after exposure, and AM were isolated and cultured. Cell viability, phagocytic activity, antioxidant response, and pro-inflammatory cytokine release were evaluated in AM cultures. After ROFA-exposure cell viability and phagocytic activity were unaltered neither in Control-AM nor in NGRAM. Whereas, Nrf2 expression and TNFα secretion increased in both Control- and NGR-AM, though the increase was lower in NGR-AM. Our studies showed that exposure to ROFA alters the defense mechanisms of AM from undernourished rats by altering Nrf2 and TNFα, essential cell mediators involved in cellular response by affectingthe immune responsiveness to air pollutants.