Elevated Blood Lead Levels in Children

Chapter 4: Cellular Biology This chapter explores altered cellular and tissue biology, focusing on cellular adaptation, injury, manifestations of cellular injury, cellular death, aging, and the various types of cell death such as necrosis and apoptosis. Cellular adaptation allows cells to respond to physiological and pathological conditions, but severe or prolonged stressors can lead to cellular injury or death. Common sources of cell injury include lack of oxygen, free radicals, infections, inflammation, and metabolic derangements. Cellular aging also contributes to changes in structure and function. Bullet points Elevated blood lead levels in children ● Children are more likely to have elevated blood lead levels ● Linked to cognitive deficits and behavioral changes ● Includes antisocial behavior, acting out in school, and attention deficits ● Deficits can persist even after exposure to lead has ended ● Lead interferes with normal remodeling of cartilage and bone in children ● Radiologic studies often reveal lead lines in children ● Lead accumulates in gums, causing hyperpigmentation ● Lead exposure during pregnancy is especially worrisome ● Can result in significant cognitive impairment and learning disabilities Treatment options ● Main methods of treatment are removal of the source of exposure ● For those with high blood lead levels, chelation therapy is used ● Additional treatment may include correcting deficiencies for iron, calcium, and zinc ● Irrigating the bowel ● Removing strategic bullets or shrapnel ● Medications for seizures Toxic effects of cadmium and arsenic ● Arsenic is found naturally in soils and water and used in various products ● Can cause acute gastrointestinal, cardiovascular, and CNS toxicities ● Chronic exposure causes skin lesions and the development of cancers ● Cadmium poisoning is a more modern problem ● Mainly due to pollution from mining, electroplating, and battery production ● Main toxic effects of excess cadmium are obstructive lung disease and renal tubular damage ● Mercury is a neurotoxic elemental metal ● Widely present in the environment and poses a global threat to health Sources of mercury exposure ● Mercury is released into the air, water, and soil through industrial processes including mining, metal and cement production, fuel extraction, and fossil fuel combustion ● Exposure sources include natural geologic sources, vehicle emissions, consumer products, industrial waste, landfills, and disposal sites ● Mercury is also found in dental amalgam, vaccine preservatives, food products, and terrestrial and marine animals consumed by humans Hazards of mercury exposure ● Debate among experts regarding the health hazards of direct mercury ingestion from the food supply or environmental vapor inhalation ● However, there is consensus on the hazards of mercury exposure during pregnancy, as it negatively impacts fetal brain development Climate change and mercury ● Thawing of frozen lands due to climate change may release long-stored mercury into lakes, rivers, and oceans Alcohol-related deaths and consequences ● Alcohol contributes to over 100,000 deaths annually, including drunk driving accidents, alcohol-related homicides, and suicides ● A blood concentration of 80 mg/dL is the legal definition for driving while intoxicated in the United States Nutritional deficiencies associated with alcohol abuse ● Major deficiencies include magnesium, vitamin B6, thiamine, folic acid, and phosphorus ● Alcohol abuse affects folic acid homeostasis, leading to deficiencies that can have serious consequences, especially during pregnancy ● Thiamine deficiencies are common in persons with alcohol abuse and can result in major neurologic sequelae Effects of alcohol on the body ● Acute effects involve the central nervous system (CNS) ● Alcohol is absorbed from the stomach and small intestine and distributed to all body tissues and fluids ● Genetic differences in alcohol metabolism and tolerance among individuals and ethnic groups ● Chronic alcoholism can lead to increased tolerance due to enhanced production of metabolic enzymes Alcohol and mortality ● Studies show an inverse association between alcohol and overall or cardiovascular mortality, including myocardial infarction and ischemic stroke ● Both irregular and chronic heavy drinking have detrimental impacts on cardiovascular health Effects of alcohol on mortality rates: ● Mortality rates tend to be lower among light to moderate drinkers (without binge drinking) compared to nondrinkers. ● Mortality rates are higher among heavy drinkers. ● Findings may be influenced by medical care and social relationships. ● Further research is recommended to understand the relationship between alcohol consumption and mortality rates. Possible cardiovascular benefits of alcohol consumption: ● Increase in high-density lipoprotein-cholesterol (HDL-C) levels. ● Decrease in low-density lipoprotein (LDL) levels. ● Prevention of clot formation. ● Reduction in platelet aggregation. ● Decrease in blood pressure. ● Increase in coronary vessel vasodilation and blood flow. ● Decrease in coronary inflammation and atherosclerosis. ● Limited ischemia-reperfusion injury. ● Decreased diabetic vessel pathology. Recommendations for alcohol consumption: ● American Heart Association recommends no more than two drinks per day for men and no more than one drink per day for women. ● One drink is defined as 12 ounces of beer, 4 ounces of wine, 1.5 ounces of 80-proof spirits, or 1 ounce of 100-proof spirits. ● Consuming alcohol in greater than recommended amounts is associated with various health hazards. ● Health hazards include increased risk for alcoholism, high blood pressure, obesity, stroke, breast cancer, suicide, and accidents. Effects of acute alcohol intoxication: ● Primarily affects the central nervous system (CNS). ● Causes dose-related CNS depression. ● Can lead to sedation, drowsiness, loss of motor coordination, delirium, altered behavior, and loss of consciousness. ● Toxic blood levels can result in a lethal coma or respiratory arrest. ● Acute alcohol intoxication may induce reversible hepatic and gastric changes.