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

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

Virtual

Encuentro; SETAC Latin America 14th Biennial Meeting; 2021

Society of Environmental Toxicology and Chemistry

Generalanalysis of the urban population health must take into account the interactionof diverse stressors such as air pollution and malnutrition. Air pollution isthe largest and most persistent environmental and public health concern inLatin American megacities. These areas are also characterized by socioeconomicgradients that enhance population inequalities, leading to malnutrition andconsequently compromising the body response to noxae. Either as a single riskfactor or in combination with other agents, air pollution causes a wide rangeof acute and chronic respiratory diseases. The respiratory system is theprincipal target of air pollution where alveolar macrophages (AM) play a keyrole providing protection against xenobiotics through a variety of mechanismsincluding oxygen dependent pathways and proinflammatory cytokine production.Oxidants could lead to a redox imbalance triggering a number of antioxidantmechanisms, of which the Nrf2-Keap1/ARE signal pathway is the most important todate. However, the mechanism linking air pollution exposure and malnutritionstill remains unclear. Based on the above, the present study sought toinvestigate the effects of exposure to ROFA (Residual Oil Fly Ash, a surrogateof urban air pollution) on the lung immune response in rat nutritional growthretardation (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 andControl rats were intranasally instilled with either 1mg/kg body weight of ROFAor 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 inAM cultures. After ROFA-exposure cell viability and phagocytic activity wereunaltered neither in Control-AM nor in NGRAM. Whereas, Nrf2 expression and TNFαsecretion increased in both Control- and NGR-AM, though the increase was lowerin NGR-AM. Our studies showed that exposure to ROFA alters the defensemechanisms of AM from undernourished rats by altering Nrf2 and TNFα, essentialcell mediators involved in cellular response by affecting the immuneresponsiveness to air pollutants.