A chemical carcinogen, 3-methylcholanthrene, alters T-cell function and induces T-suppressor cells in a mouse model system.

The in-vivo effects of a polycyclic aromatic hydrocarbon (PAH), 3-methylcholanthrene (MCA), on in-vitro mitogen activation, cell-mediated lympholysis (CML) and T-cell subset distribution in mouse splenic lymphocyte populations were measured. Three inbred mouse strains were treated with a single intraperitoneal injection of corn oil alone or with different doses of MCA in oil (0.5-50 mg kg -1). One to ninety days after injection, splenic lymphocytes were isolated, and assayed for blastogenesis, CML and the percent T-helper and T-suppressor cells using monoclonal antibodies. High doses of MCA suppressed mitogen activation (15.2-53.6%) and CML (69-90%) within 24 hr in lymphocytes from PAH-responsive mice (C57 and C3H). Blastogenesis was stimulated and CML was suppressed to a lesser degree (5-45%) in lymphocytes from non-responsive mice (DBA). MCA induced an increase in T-suppressor cells in responsive mice, but there was no change in DBA mice. These studies suggest a correlation between immunocytotoxicity of PAH compounds on T-cell subsets and the responsiveness of mouse strains to these carcinogens

Intrauterine exposure to fine particulate matter as a risk factor for increased susceptibility to acute broncho-pulmonary infections in early childhood

Over the last decades many epidemiologic studies considered the morbidity patterns for respiratory diseases and lung function of children in the context of ambient air pollution usually measured in the postnatal period. The main purpose of this study is to assess the impact of prenatal exposure to fine particulate matter (PM(2.5)) on the recurrent broncho-pulmonary infections in early childhood. The study included 214 children who had measurements of personal prenatal PM(2.5) exposure and regularly collected data on the occurrence of acute bronchitis and pneumonia diagnosed by a physician from birth over the seven-year follow-up. The effect of prenatal exposure to PM(2.5) was adjusted in the multivariable logistic models for potential confounders, such as prenatal and postnatal ETS (environmental tobacco smoke), city residence area as a proxy of postnatal urban exposure, children’s sensitization to domestic aeroallergens, and asthma. In the subgroup of children with available PM(2.5) indoor levels, the effect of prenatal exposure was additionally adjusted for indoor exposure as well. The adjusted odds ratio (OR) for incidence of recurrent broncho-pulmonary infections (five or more spells of bronchitis and/or pneumonia) recorded in the follow-up significantly correlated in a dose-response manner with the prenatal PM(2.5) level (OR = 2.44, 95%CI: 1.12 – 5.36). In conclusion, the study suggests that prenatal exposure to PM(2.5) increases susceptibility to respiratory infections and may program respiratory morbidity in early childhood. The study also provides evidence that the target value of 20 μg/m(3) for the 24-hour mean level of PM(2.5) protects unborn babies better than earlier established EPA guidelines