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. 2022 May 10;1(1):31–45. doi: 10.1016/j.eehl.2022.04.003

Table 2.

Toxicological evidence on the potential pathogenicity of environmental pollutants.

Type Chemical Biological effects/potential mechanism References
Heavy metals and organometallic compounds Cadmium (Cd) Cause liver diseases such as oxidative stress, fibrosis, and lipid deposition. [[155], [156], [157], [158], [159], [160], [161], [162]]
Induce osteoporosis and osteomalacia. [163,164]
Reproductive toxicities such as premature delivery and fetal growth inhibition. [[165], [166], [167]]
Lead (Pb) Neurotoxic effects, including the influence of hippocampal neurogenesis and functional plasticity, defects of learning and memory in offspring mice, and cognitive deficits in later life among rodents and primates. [[170], [171], [172], [173]]
Methylmercury (MeHg) High neurotoxic effects, including mitochondrial dysfunction, behavioral changes, and blood–brain barrier damage. [[175], [176], [177], [178], [179]]
Organic halogen compounds Tetrabromobisphenol A (TBBPA) Thyroid morphological abnormalities and thyroid dysfunction [182]
Neurotoxic effects, including impairment of spatial learning ability and activity habits in adult rats, the impact of Ca2+ imbalance, amino acid receptors and oxidative stress in SH-SY5Y cells, and damage of the blood–brain barrier. [181,183,184]
Hepatorenal toxicity in rodents. [185,186]
Polychlorinated biphenyls (PCBs) Endocrine-disrupting effects such as (ant)agonistic activities of ER. [187,188]
Neurobehavioral toxic effects, including longer reflexes and anxious behaviors in offspring mice. [189,190]
Reproductive toxicities such as affect semen quality in male rats. [191]
Per- and polyfluoroalkyl substances (PFASs) Neurotoxic effects such as increased motor activity and decreased habituation in offspring, impaired spatial memory and learning, and neurological dysfunction and neurobehavioral changes in rodents. [[193], [194], [195], [196]]
Reproductive toxicities, including the influence of oocyte quality and fertilization failure in pig. [197]
Endocrine-disrupting effects such as interference with the human thyroid hormone system. [198,199]
Hematotoxicological effects by perturbing the plasma kallikrein-kinin system (KKS) and increasing the permeability of vascular endothelial cells. [200,201]
Phenolic and bisphenolic compounds Bisphenol A (BPA) Endocrine-disrupting effects, including the agonistic activity of ER and antagonistic activities of AR, TR, and PPARγ. [[205], [206], [207], [208], [209]]
Reproductive toxicities such as reducing adult sexual activity levels, promoting sexual maturation, affecting the menstrual cycle, and inhibiting embryonic development in female rodents, and also affecting the meiosis process of spermatocytes in male rodents. [[210], [211], [212], [213]]
Neurotoxic effects such as behavioral abnormalities, neuronal apoptosis, and cognitive decline. [[214], [215], [216]]
Synthetic phenolic antioxidants (SPAs) Lipid metabolism disorders such as promoting the adipogenic differentiation of 3T3-L1 preadipocytes and accelerating the accumulation of intracellular triglycerides in mice. [219,220]
Endocrine-disrupting effects such as perturb steroidogenesis. [221]
Reproductive toxicity such as weight reduction of uterine and uterine adnexa in immature female rats. [222]
Airborne fine PMs PM2.5 Cause cardiovascular and respiratory problems. [226]
Neurotoxic effects such as induced cellular damage in SH-SY5Y cells and compromised learning and cognitive performance. [227,228]
Reproductive toxicity such as reducing the serum testosterone levels, the sperm count and motility, and promoting the sperm malformation and germ cell apoptosis in male SD rats. [[229], [230], [231]]
Metabolism disorders of glucose and lipid such as impaired glucose tolerance, hindered glycogen synthesis, increased plasma glucose levels, and induced inflammatory response of visceral adipose tissue and liver lipid metabolism in male mice. [232,233]