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Smoking during pregnancy is directly associated with numerous serious conditions, such as premature birth, low birth weight, and perinatal mortality. We quantitatively evaluated histological inflammatory alterations, oxidative damage by lipid peroxidation, the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) in the lungs of mice exposed to cigarette smoke during pregnancy. Eight female and four male mice were mated for five days. Pregnant female mice were randomly allocated to the control group or to the cigarette smoke group (n = 8) in which they were exposed to 12 cigarettes per day in an exposure chamber, three times a day for 21 days. The control group (CG; n = 8) was kept in the exposure chamber for the same duration, but without exposure to cigarette smoke. Six newborn mice from both groups were weighed 24 hours after birth and then euthanized. Lung tissue was collected and subjected to histomorphometric and biochemical analyses. The cigarette smoke group showed a significant reduction in snout-vent length compared to the control group. Histomorphometric analysis indicated increased alveolar septal thickness and a larger alveolar lumen in mice exposed to cigarette smoke than in mice in the control group. We observed increased alveolar inflammatory infiltrate, decreased SOD activity, and significantly higher oxidative damage in the cigarette smoke group. Our data indicate that cigarette smoke exposure during pregnancy decreases body length at birth, changes lung tissue, and causes redox imbalance and histological damage in newborn mice.

Chloroform is an organic solvent used as an intermediate in the synthesis of various fluorocarbons. Despite its widespread use in industry and agriculture, exposure to chloroform can cause illnesses such as cancer, especially in the liver and kidneys. The aim of the study was to analyze the effects of chloroform on redox imbalance and pulmonary inflammatory response in adult C57BL/6 mice. Forty animals were divided into 4 groups (N = 10): female (FCG) and male (MCG) controls, and females (FEG) and males (MEG) exposed to chloroform (7.0 ppm) 3 times/d for 20 minutes for 5 days. Total and differential cell counts, oxidative damage analysis, and protein carbonyl and antioxidant enzyme catalase (CAT) activity measurements were performed. Morphometric analyses included alveolar area (Aa) and volume density of alveolar septa (Vv) measurements. Compared to FCG and MCG, inflammatory cell influx, oxidative damage to lipids and proteins, and CAT activity were higher in FEG and MEG, respectively. Oxidative damage and enzyme CAT activity were higher in FEG than in FCG. The Aa was higher in FEG and MEG than in FCG and MCG, respectively. The Vv was lower in FEG and MEG than in FCG and MCG, respectively. This study highlights the risks of occupational chloroform exposure at low concentrations and the intensity of oxidative damage related to gender. The results validate a model of acute exposure that provides cellular and biochemical data through short-term exposure to chloroform.