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Plastic is synonymous with modern life.
However, the plastic products that people often use can be harmful.
The existing literature indicates that daily use of plastic products may cause cardiovascular and endocrine diseases.
Plastic is everywhere Plastic is one of the most widely used materials in the world, from mineral water bottles to large jet aircraft.
The use of plastics has expanded to food packaging, toys, clothing, electronic products, safety equipment and other fields.
Plastics are widely used in clinics, such as various disposable sterile products (blood storage bags, syringes, catheters, etc.
).
Medical plastics can also improve the durability and biocompatibility of implantable devices (such as heart valves, stents, and pacemakers).
Plastic products are made of synthetic polymer materials mixed with chemical additives (such as plasticizers and colorants) and molded under heating.
In recent years, people have been concerned about the health effects of plastic exposure.
Concerns are mainly focused on additives such as plasticizers, such as bis(2-ethylhexyl) phthalate (DEHP) and bisphenol A (BPA).
The impact of DEHP and BPA on the human body Soon after World War II, DEHP began to be used in the medical field.
Surgeon and inventor Carl Walter used DEHP to create plastic blood bags.
These new, soft blood bags are easier to transport than glass and can withstand steam sterilization, thereby reducing bacterial contamination.
Since DEHP is not covalently bound to polyvinyl chloride, DEHP is easily leached from plastic materials, exposing the human body to a large amount of DEHP.
In the 1950s, it was discovered that BPA monomer can be used to make transparent and durable polycarbonate plastic or epoxy resin for protective coating (such as canned food).
However, subsequent studies have shown that incomplete polymerization or degradation of BPA-containing products can lead to human exposure to BPA (this compound is now considered a carcinogen).
This discovery has attracted the attention of consumers, and the use of BPA in baby bottles and baby food packaging has been discontinued.
However, BPA and DEHP are still produced in large quantities and are used in the production of various consumer and medical products.
DEHP and BPA are everywhere, and biological monitoring studies have reported that DEHP and BPA levels can be detected in 75%-90% of the general population.
In addition, the medical environment can lead to increased exposure to these chemicals.
For example, a study reported that urinary BPA (42%) and DEHP metabolites (1500%-2100%) concentrations of pediatric patients after cardiac surgery continued to increase within a few hours to several weeks after surgery.
In addition, DEHP and BPA exposure can affect endocrine, which can change hormone homeostasis and signal transduction pathways.
A 10-year longitudinal study found that compared with low BPA exposure, high BPA exposure was associated with a 46%-49% increase in the risk ratio of cardiovascular death and all-cause mortality.
Previous epidemiological research reports have shown that elevated urine DEHP or BPA levels are associated with increased risks of coronary and peripheral artery disease, chronic inflammation, myocardial infarction, angina pectoris, and hypertension.
The correlation with hypertension is further supported by data from a randomized controlled trial, which found that compared with subjects using glass containers, the use of cans with BPA on the inner wall caused a sharp increase in urine BPA levels and increased systolic blood pressure.
There is a direct link between about 4.
5 mmHg.
Mechanism: Why does plastic have cardiovascular toxicity? The causes of the toxicity of DEHP and BPA to the cardiovascular system may be various.
At present, inflammation, oxidative stress and hormone imbalance are considered as potential factors.
For example, an observational study showed that premature infants who received intravenous fluids had elevated DEHP levels.
Patients with high DEHP levels are at increased risk of developing essential hypertension, which is related to the imbalance of cortisol (a glucocorticoid).
In population and epidemiological studies, it may be difficult to determine the cause of the disease, but experimental work has clearly shown that there is a direct link between plastic chemicals and cardiac insufficiency.
For example, BPA exposure can disrupt the signal transduction of cardiac calcium ions, which are important regulators of electrical activity, contractile function, and vascular activity.
Acute BPA exposure can inhibit voltage-gated calcium channels and damage intracellular calcium activity in mouse cardiomyocytes and isolated mouse heart tissues.
It is worth noting that the described effects are largely reversible, indicating that BPA can directly interact with calcium channels or calcium cycle-related regulatory proteins.
In addition, the effects of BPA may be sex-specific and directly related to estrogen activity, because these effects are largely negated in mouse models of loss of estrogen receptor function.
DEHP is considered a heart depressant.
Acute exposure to DEHP or its main metabolite mono(2-ethylhexyl) phthalate can reduce the blood flow and contractile tension of the coronary arteries of the rat heart, and reduce the contractile function of the atria.
In addition, phthalates can slow the heart rate, atrioventricular conduction, and epicardial conduction velocity.
The negative inotropic effects of phthalates may be mediated through interactions with muscarinic receptors, and disruption of gap junctions can slow down electrical conduction.
Importantly, gap junction uncoupling exists in other organ systems exposed to phthalates (such as the male reproductive tract and liver).
It is too late to stop using plastics, and it is uncertain whether these experimental results are fully applicable to humans.
In view of the ubiquity of plastics, efforts are needed in the future to work together to bridge the gap between experimental, epidemiological, and clinical investigations to determine the impact of plastics on cardiovascular health.
Literature index: Posnack, NG Plastics and cardiovascular disease.
Nat Rev Cardiol, 2021; 18: 69–70.
However, the plastic products that people often use can be harmful.
The existing literature indicates that daily use of plastic products may cause cardiovascular and endocrine diseases.
Plastic is everywhere Plastic is one of the most widely used materials in the world, from mineral water bottles to large jet aircraft.
The use of plastics has expanded to food packaging, toys, clothing, electronic products, safety equipment and other fields.
Plastics are widely used in clinics, such as various disposable sterile products (blood storage bags, syringes, catheters, etc.
).
Medical plastics can also improve the durability and biocompatibility of implantable devices (such as heart valves, stents, and pacemakers).
Plastic products are made of synthetic polymer materials mixed with chemical additives (such as plasticizers and colorants) and molded under heating.
In recent years, people have been concerned about the health effects of plastic exposure.
Concerns are mainly focused on additives such as plasticizers, such as bis(2-ethylhexyl) phthalate (DEHP) and bisphenol A (BPA).
The impact of DEHP and BPA on the human body Soon after World War II, DEHP began to be used in the medical field.
Surgeon and inventor Carl Walter used DEHP to create plastic blood bags.
These new, soft blood bags are easier to transport than glass and can withstand steam sterilization, thereby reducing bacterial contamination.
Since DEHP is not covalently bound to polyvinyl chloride, DEHP is easily leached from plastic materials, exposing the human body to a large amount of DEHP.
In the 1950s, it was discovered that BPA monomer can be used to make transparent and durable polycarbonate plastic or epoxy resin for protective coating (such as canned food).
However, subsequent studies have shown that incomplete polymerization or degradation of BPA-containing products can lead to human exposure to BPA (this compound is now considered a carcinogen).
This discovery has attracted the attention of consumers, and the use of BPA in baby bottles and baby food packaging has been discontinued.
However, BPA and DEHP are still produced in large quantities and are used in the production of various consumer and medical products.
DEHP and BPA are everywhere, and biological monitoring studies have reported that DEHP and BPA levels can be detected in 75%-90% of the general population.
In addition, the medical environment can lead to increased exposure to these chemicals.
For example, a study reported that urinary BPA (42%) and DEHP metabolites (1500%-2100%) concentrations of pediatric patients after cardiac surgery continued to increase within a few hours to several weeks after surgery.
In addition, DEHP and BPA exposure can affect endocrine, which can change hormone homeostasis and signal transduction pathways.
A 10-year longitudinal study found that compared with low BPA exposure, high BPA exposure was associated with a 46%-49% increase in the risk ratio of cardiovascular death and all-cause mortality.
Previous epidemiological research reports have shown that elevated urine DEHP or BPA levels are associated with increased risks of coronary and peripheral artery disease, chronic inflammation, myocardial infarction, angina pectoris, and hypertension.
The correlation with hypertension is further supported by data from a randomized controlled trial, which found that compared with subjects using glass containers, the use of cans with BPA on the inner wall caused a sharp increase in urine BPA levels and increased systolic blood pressure.
There is a direct link between about 4.
5 mmHg.
Mechanism: Why does plastic have cardiovascular toxicity? The causes of the toxicity of DEHP and BPA to the cardiovascular system may be various.
At present, inflammation, oxidative stress and hormone imbalance are considered as potential factors.
For example, an observational study showed that premature infants who received intravenous fluids had elevated DEHP levels.
Patients with high DEHP levels are at increased risk of developing essential hypertension, which is related to the imbalance of cortisol (a glucocorticoid).
In population and epidemiological studies, it may be difficult to determine the cause of the disease, but experimental work has clearly shown that there is a direct link between plastic chemicals and cardiac insufficiency.
For example, BPA exposure can disrupt the signal transduction of cardiac calcium ions, which are important regulators of electrical activity, contractile function, and vascular activity.
Acute BPA exposure can inhibit voltage-gated calcium channels and damage intracellular calcium activity in mouse cardiomyocytes and isolated mouse heart tissues.
It is worth noting that the described effects are largely reversible, indicating that BPA can directly interact with calcium channels or calcium cycle-related regulatory proteins.
In addition, the effects of BPA may be sex-specific and directly related to estrogen activity, because these effects are largely negated in mouse models of loss of estrogen receptor function.
DEHP is considered a heart depressant.
Acute exposure to DEHP or its main metabolite mono(2-ethylhexyl) phthalate can reduce the blood flow and contractile tension of the coronary arteries of the rat heart, and reduce the contractile function of the atria.
In addition, phthalates can slow the heart rate, atrioventricular conduction, and epicardial conduction velocity.
The negative inotropic effects of phthalates may be mediated through interactions with muscarinic receptors, and disruption of gap junctions can slow down electrical conduction.
Importantly, gap junction uncoupling exists in other organ systems exposed to phthalates (such as the male reproductive tract and liver).
It is too late to stop using plastics, and it is uncertain whether these experimental results are fully applicable to humans.
In view of the ubiquity of plastics, efforts are needed in the future to work together to bridge the gap between experimental, epidemiological, and clinical investigations to determine the impact of plastics on cardiovascular health.
Literature index: Posnack, NG Plastics and cardiovascular disease.
Nat Rev Cardiol, 2021; 18: 69–70.
