The occurrence of disorders of glucolipid metabolism from the initial influence of genetic and environmental factors to the gradually recognized chronic low-grade inflammation, the multifaceted regulation of psychiatric, dietary, and dysbiosis factors, has built us a neuro-endocrine-immune-inflammatory regulatory network, and environmental endocrine is inextricably linked to any link of this network. In this paper, the effects of air pollutant particles, diphenol A, mental stress, and light pollution on metabolic disorders will be described in terms of air pollution, food additives, neuropsychiatric factors, and altered biological cycles. 1, the impact of air pollutant particles on human metabolism Air pollutant particles seriously affect human health has been recognized, air particulate matter (PM) is a general term for solid and liquid particulate matter in the atmosphere. According to its particle size, it can be divided into coarse dispersion system (particle size > 10Lm) and colloidal dispersion system (0. 01~10Lm). Among them, particle size 0. 1~10Lm is respirable particulate matter, which is also the most hazardous particulate matter to human health. With the process of industrialization and urbanization, the emission of automobile exhaust, industrial waste gas, residential waste gas and construction, the concentration of some pollutants in the atmosphere has increased significantly, such as PM2.5, PM10, NO2, SO2, CO, etc. Among them, the impact of PM2.5 on endocrine and metabolism is getting more and more attention. It is also called fine particulate matter. Because PM 2.5 can enrich and carry many carcinogenic and toxic substances, such as PAHs, heavy metals, etc., the hot spot of PM research in recent years is gradually shifting from the study of coarse particles (PM10) to fine particles (PM215) and even ultrafine particles. Most of the harmful elements and compounds are enriched in fine particles, and as their particle size decreases, the retention time of fine particles in the atmosphere and the absorption rate in the respiratory system as well as the impact on the endocrine system also increase, and the greater the impact on human health. It has been suggested [1] that when the atmospheric PM10 and PM2.5 concentrations increase by 10ug/m3, the total number of deaths increases by 0.53% (0.22%- 0.85%) and 0.85% (0.32%-1.39%), respectively. Churg et al. found that 96% of the particles deposited in the lung parenchyma were PM2.5, suggesting that the lung has a high retention selectivity for particles in this particle size range. The correlation analysis between PM2.5 and PM10 pollution and the number of respiratory and pediatric respiratory clinics during the haze period in Shanghai [3] showed that the average daily number of respiratory and pediatric respiratory clinics increased by 3% and 0.5%, respectively, for every 50 μg/m3 increase in the daily average PM10 concentration on the day of the haze; the average daily number of respiratory and pediatric respiratory clinics increased by 3.2% and 0.5%, respectively, for every 34 μg/m3 increase in the daily average PM 2.5 concentration. The lagged cumulative effect of PM 2.5 and PM10 pollution on the number of outpatient clinics was greater than the daily effect, and the cumulative effect was maximized on day 6d of the haze pollution outbreak. PM2.5 concentrations are not constant throughout the year, and some scholars have monitored PM 2.5 in six Brazilian cities and found that PM 2.5 concentrations are lower in the southern hemisphere during the summer months (November to February). Epidemiological surveys suggest that people with diabetes are susceptible to particulate pollution, and Alexandra Schneider found that exposure to PM2.5 particles can cause damage to the cardiovascular and hematological systems, especially in older patients with cardiovascular disease. The study took 22 type 2 diabetic patients (mean age 61 years) as subjects and used systemic inflammation, blood clotting, and autonomic heart rhythm as indicators to study the effects of short-term exposure to PM2.5. The results showed that obese diabetic populations, and those with elevated glycosylated hemoglobin, low lipocalin, high ferritin, or glutathione transferase M1 null genotype had higher IL-6 levels in repolarization after 4 days of exposure in the absence of treatment with beta-blockers. This suggests that exposure to a higher PM2.5 environment alters the repolarization of vascular cells, with the result that it may raise the risk of heart failure and lead to arrhythmias. Exposure to PM2.5 also raises the level of systemic inflammatory response, with insulin resistance and oxidative stress reinforcing the effects between the two. Most epidemiological studies of pollutants now rely on ground-based detection networks, but ground-based detection of PM2.5 is often limited by, for example, the uneven spatial distribution of pollutants, and satellite continuum analysis of the relationship between land surface aerosol optical thickness (AOD) and PM2.5 has also shown a correlation between coronary heart disease and PM2.5 exposure. However, it has also been shown that short-term exposure to PM2.5 does not increase the probability of ischemic stroke . 2. The effect of BPA on human metabolism Endocrine D isruptors (EDs) are a class of exogenous compounds or mixtures that can alter the function of the endocrine system, thereby negatively affecting the organism as a whole, its offspring and populations. The role of endocrine disruptors, represented by bisphenol a, in the development of diabetes and obesity cannot be ignored. Obesity and diabetes have become global health problems, and genetic and environmental factors are the causes of diabetes and obesity, with the development of socio-economic level, environmental factors play an important role more and more, statistics show that there are about 1 billion overweight adults and 300 million obese people in the world. Among the world’s adult population aged 20-79 years, the proportion of diabetic patients is about 6.4%. Bisphenol A (BPA), as a chemical material, is widely used in plastic packaging, milk bottles, plastic containers, etc. It is a disruptor that can affect human endocrine and metabolism. relationship, and found that urinary BPA levels were significantly associated with overweight, generalized obesity, abdominal obesity and insulin resistance in the middle-aged and elderly population. The results suggest that people should minimize the exposure to BPA in daily life. On April 18, 2008, Canadian health authorities announced a ban on the use of BPA-containing plastics in baby bottles, the first country in the world to decide to restrict the use of the compound because of evidence of disturbing effects of BPA. However, there is still intense debate among academics and regulators about the dangers of most environmental pollutants and the need for action. A large epidemiological survey conducted in the United States found that the higher the concentration of BPA in urine, the higher the chance of cardiovascular disease, diabetes, and liver disease. 3, the impact of environmental estrogen on the human body Environmental endocrine disruptors, the most estrogen-like chemicals, also known as “environmental estrogen”. These substances are similar in structure or function to endogenous estrogens and can affect the development of the reproductive system. Although high calorie food intake and reduced exercise are the main environmental triggers of obesity and diabetes, the induction of obesity and diabetes by environmental endocrine disruptors is not negligible, and estrogen levels also play an important role in the brain’s regulation of body weight and energy metabolism. In a study of Syrian hamsters, estrogen exposure was found to reduce body weight and fat content, but not food intake. Treatment with tamoxifen attenuated this effect of estrogen, and knockdown of the estrogen receptor ERA gene in mice resulted in weight gain and insulin resistance, suggesting that estrogen receptor-mediated regulatory pathways play an important role in the development of obesity. The use of estrogen therapy in overweight or obese young postmenopausal women can reduce fat accumulation and improve body fat distribution, suggesting that endogenous estrogens can promote fat degradation. Some exogenous estrogenic active compounds may be associated with the production of adipose tissue. There are more than 80 types of hormones, which can be classified into four major categories according to their sources: natural estrogens, phytoestrogens, animal estrogens, and synthetic estrogens. Natural estrogens mainly include estradiol, estrone and estriol, among which estradiol has the strongest effect. According to a survey in Shanghai, the prevalence of precocious puberty in children in the city has reached 1%. The onset of precocious puberty in children is related to the influence of estrogen. With the application of additives in feed, the growth cycle and market time of animals are shortened, but some additives remain in animals and affect human health through the accumulation effect of the food chain. The long-term use of such animal estrogen-containing foods in children may be one of the causes of precocious puberty. In addition, certain phytoestrogens, such as soy-derived isoflavones, may also affect the hypothalamic-pituitary-gonadal axis when consumed for long periods of time. Endocrine disruptors can also affect the thyroid axis. Excessive intake of soy products during infancy increases the incidence of autoimmune thyroid disease during adolescence. Certain industrial ingredients have estrogen-like effects, such as PCB compounds and phthalates have also been found to have estrogen-like effects. Polychlorinated biphenyls are widely used in electronics. Phthalates are plasticizers in the production of plastics and rubber, and they enable better dispersion of oil-phase substances in the aqueous phase. Exposure to phthalates during fetal life may impair testicular function and shorten the anus-testis spacing after birth. Plasticizers, which have similar effects to “clouding agents,” are banned from food additives and plastic food packaging, and replacing edible “clouding agents” with relatively inexpensive plasticizers can cause chronic toxic damage to humans. Children’s metabolic rate is faster and their exposure to toxic and harmful substances through the “hand-to-mouth route” is higher, so children’s long-term exposure to environmental estrogens can easily cause pseudobreast development and precocious puberty. Phthalates are widely used in female care products such as perfumes, hair dyes, nail polish, and body odor removers. A foreign study found that the relationship between urinary phthalate metabolite concentrations and care products was observed in 337 women who used 13 care products (PCP) during 2002-2005 with 3-36 months follow-up, and a linear regression analysis was done, and it was found that women who used PCP, especially perfume or fragrance products, had elevated urinary concentrations of multiple dimethyl phthalate The concentrations of metabolites were elevated. Women exposed to phthalates during pregnancy may have effects on the fetus and, at the same time, increase their own risk of developing AD and LEI. Taiwanese scholars found that girls with early breast development had higher levels of MMP ((96.5 ~ 134.0 ng/ml)) than controls ((26.4 ~ 30.0 ng/ml)), suggesting that phthalates have an effect on adolescent girls.