Table 2.

The effect of PM_2.5 exposure on endocrine systems of the male and female individuals.

Serial No.	Exposure type	Study participants	Toxic effects	Reference
1.	PM2.5 at 3.7 μg/m3	Prenatal exposure	increased neonatal TSH levels	(77)
2.	Ambient PM2.5 at 8.13 µg/m3 concentration	Salivary cortisol output during pregnancy in a	decline in cortisol throughout the day with increasing exposure	(78)
3.	NO2 at 24.4 ± 14.0 ppb and PM2.5 at 55.6 ± 41.5 μg/m3/day for 1-14 days	COPD patients to the neuroendocrine response in COPD patients.	Increase in CRH, ACTH, and norepinephrine, and decreases in cortisol and epinephrine	(79)
4.	PM2.5	Prenatal exposure during third trimester of pregnancy	Increased depression risk and induces activation of the HPA axis	(80)
5.	PM2.5	Young adolescent girls	heightened HPA-axis stress responsivity, Increased biological sensitivity to social stress	(60)
6.	PM2.5	Exposure during pregnancy	Dose dependent increase in cortisol levels in cord blood, as the distance of exposure increased, the decrease in cord-blood cortisol level	(81)
7.	10 ppb of NO2, PM2.5	45-85 years old participants	9.7% higher wake-up cortisol associated with a 10 ppb NO2, the cortisol curve became flatter over 5 years.	(82)
8.	PM2.5 at 41.1 μg/m3	Young adults	NO3 ion was still significantly associated with CRH, Increased CRH, ACTH and cortisol.	(83)
9.	PM2.5	Pregnant individuals	first-trimester exposures were associated with mild thyroid dysfunction throughout pregnancy, dose dependent increase in toxicity	(84)
10.	PM2.5	Elderly women with mean age of 73.5 ± 3.0 years	Higher risk of dementia in women with three estrogen receptors with SNPs	(85)
11.	PM2.5, O3 and NO2	Air pollutants and hormone-assessed pubertal development	No statistical effect on hormone levels of E2 and testosterone	(86)
12.	Three-years exposure to PM2.5	Dementia-free women aged 80 and older	episodic memory declines mediated by depressive symptoms	(87)
13.	PM2.5	Black women	not associated with a higher risk of breast cancer except for some geographic areas	(88)
14.	PM2.5	Pre-conception and early prenatal periods	can lead to altered steroid adaptation during the state of pregnancy	(89)
15.	PM2.5, NO2	Women with 1-year familial breast cancer risk	Increased risk among women with a higher familial risk with NO2 only	(52)
16.	Improved air quality with PM2.5	Exposure for 3 years in older women of less or more than 80 years with no dementia	improvement in long-term AQ in late life was associated with slower cognitive declines in older women	(90)
17.	NO2, CO, SO2, or PM2.5, PM10	Female adults aged ≥ 40 years	Increased risk of osteoporosis in female with PM10 only	(91)
18.	PM2.5	All cause ovarian cancer patients 18–79 years	PM2.5 concentrations were associated with an increased risk of all-cause mortality.	(92)
19.	PM2.5 4.9 to 17.5 µg/m3	31 years old female participants	Weak inverse associations with POM, no dose response relationships	(93)
20.	PM2.5 and PM10 through road exposure	150 mother-newborn pairs	Directly related to increased cortisol levels in cord-blood	(81)
21.	NO2 at 10 ppb and PM2.5	45–85 years old participants	Higher wake-up salivary cortisol with NO2 only which flattened over 5 years	(82)
22.	PM2.5 in residential areas	Women in third trimester of pregnancy	More severe depressive symptoms and activation of HPA axis	(80)
23.	NO2, O3 and PM2.5	Obese Latino children and adolescents	Higher O3 exposure caused higher morning cortisol PM2.5 exposure (4–10 months) caused lower serum morning cortisol.	(94)
24.	PM2.5 at 41.1 μg/m3	CRH, ACTH and cortisol in young adults	Water-soluble inorganic constituents especially, NO3, caused stronger activation of HPA axis	(83)
25.	PM2.5, PM10	Participants from couples who underwent in-vitro fertilization treatment	PM2.5 increased seminal testosterone and malondialdehyde, and reduced sperm progressive motility.	(95)
26.	PM2.5	Prenatal exposure to pregnant individuals	Reduced anogenital distance of new born	(96)
27.	PM2.5	Pregnant individuals in third trimester	Increased in cord blood levels of 17α-hydroxy-pregnenolone	(97)
28.	PM2.5, SO2 and CO	women undergoing assisted reproductive procedure	Reduced testosterone, progesterone and FSH	(98)
29.	PM2.5, NO2, SO2, CO, and O3	Effect on testosterone, FSH, LH, E2, PRL in men aged 20–55 years	immediate and short-term cumulative PM2.5 reduced testosterone.	(99)
30.	PM2.5, NO2 and PM10	infertile men	PM2.5, and NO2 were negatively associated with sperm morphology.	(100)
31.	PM1, PM2.5, and PM10	Rural adult male and female	PM2.5 increased the testosterone in male and reduced progesterone in both male and female.	(101)
32.	PM2.5 particles and bound eight PAHs	Male college students	LMW-PAHs negatively affected sperm morphology, PAHs increased sperm motility.	(102)
33.	single-day and cumulative effects of air pollutants of PM2.5, SO2, and NO2	Male young adults	PM2.5 concentrations were positively associated with E2. SO2 and O3 reduced E2.	(103)
34.	PM2.5, CO, NO2, PM10	Infertile men	PM2.5, CO and NO2 were negatively associated with the level of testosterone, PM2.5 also caused immature chromatin	(104)
35.	PM2.5	fertile men of 20-45 years	Decreased sperm motility, total motility, and sperm quality	(105)
36.	PM2.5, PM10, SO2, NO2, CO, and O3 14-18 µg/m3 During the third trimester	Women with preterm birth information or low-birth weight	Low birth weight risk was associated with PM2.5, NO2, and O3	(42)

ACTH, adrenocorticotropic hormone; CRH, Increased corticotropin releasing hormone; COPD, Chronic obstructive pulmonary disease; E2, Estradiol; FSH, follicle stimulating hormone; HPA, Hypothalamus pituitary axis; LH, luteinizing hormone; LMW, low molecular weight; PAH, Poly aromatic amines; POM, Polycystic ovarian morphology; PRL, prolactin; SNP, Single nucleotide polymorphism.