Environmental Diseases
Bill Becker, DO, MPH
Clinical Associate Professor Dept of Pathology Ohio State University
Objectives – Selected Environmental Diseases
Chemical agents – therapeutic & nontherapeutic
– Lead
Physical agents - burns Radiation injury Nutritional diseases
– Protein energy malnutrition – Vitamin Deficiencies
General – Environmental Disorders
Injuries/disorders caused by chemical or physical agents Related field – Occupational medicine – injuries that occur in the workplace Regulatory agencies – EPA, FDA, OSHA, Consumer Products Safety Commission
General – Environmental Disorders
Air pollution – both indoor & outdoor Industrial exposures – coal, asbestos, metals Tobacco smoke (don‟t smoke – please!) Chemical agents Physical agents Electrical injury Radiation injury Nutritional diseases
Injury from Chemical Agents
Occur by inhalation, ingestion, injection or absorption thru the skin Est. 2 million exposures/yr in the US Kids account for 61% Common house items – cleaners, analgesics, cosmetics, plants, cold meds CLADME
Injury by Therapeutic Agents
Averse drug reactions are common (2%) Relatively minor ADR‟s – rashes, GI upset Major - anaphylaxis (penicillin is classic), blood clots, arrhythmias, hematologic (anemia, thrombocytopenia, leukopenia) ADR‟s are also related to potency – anticancer meds
Injury by Therapeutic Agents
Aspirin – overdose may be accidental (kids) or intentional (adolescents/adults) Acetaminophen – OD with large ingestions (15-20 gms) – causes liver damage, may result in liver failure/death
Injury by Therapeutic Agents
Exogenous Estrogens – until 2002 HRT widely used for menopausal symptoms and prevention of osteoporosis Recent Women‟s Health Initiative data – long term use has ↑‟er risk of heart disease, breast ca, strokes & blood clots Short term use may have better risk-benefit relationship OCP‟s also have risks & benefits that should always be considered
Injuries by Non-therapeutic Agents Lead
Lead is found in urban air, soil, water, food, house dust, batteries, older paints & gasoline Occupational lead – mining, foundries 85% of Pb is taken up by bones & teeth – it competes with Ca++ and interferes with remodeling process. “Lead lines” Hyperpigmented gums – „blue line‟
Radiodense metaphyseal lines – lead poisoning
Lead
Pb blocks or hinders incorporation of Fe++ into hemoglobin *** Develop anemia (microcytic, hypochromic) Neurologic disturbances – range from mild to learning difficulties to sensory & motor deficits Wristdrop and footdrop (adults)
Lead
GI tract – colicky pain – severe, not localized Kidneys – damages tubules, fibrosis, perhaps even renal failure Public Health & EPA monitor Pb (10 g/dL)
– African American kids (11.2%) – Caucasian kids (2.3%)
Chelation therapy
Drugs of Abuse (Non-therapeutic)
Sedative-hypnotic – EtOH, barbiturates, benzodiazepines CNS Stimulants – cocaine, amphetamines Opioids – heroin, morphine, methadone, codeine
Hallucinogens – LSD, PCP, mescaline, MDMA Inhalants – glue, toluene, paint thinner, gasoline, amyl nitrate, nitrous oxide Nonprescription drugs – analgesics, antihistamines, scopolamine, atropine
Club Drugs
Used in bars, dance clubs, raves, trances Methamphetamines, LSD, Ketamine, MDMA (ecstasy), GHB, Rohypnol Bruxism – clenching of teeth – use of “e”
Physical Agents
Mechanical trauma – abrasions, contusions, lacerations, incisions, puncture wounds Thermal injuries – body operates in temperature range of 31o to 41oC (89-106oF) Hyperthermia (burns) – cause > 5000 deaths/yr in the US Hypothermia – due to prolonged exposure to low temps
Burns – Important Factors ***
% of body surface area (rule of 9‟s)
– Head & neck 9% – Trunk front 18%, trunk back 18% – Arms 9% each (hands are 1% each) – Legs 18% each – Perineum 1 %
Burns – Important Factors ***
Depth of the burn (full or partial thickness) Potential for internal injuries from inhalation of fumes or hot gases Age of the patient (elderly & very young) How fast and how well is it treated?
Clinical Consequences of Burns
If > 50% bsa involved – grave prognosis Shock common when > 30-40% bsa involved
– Massive fluid shifts – hypovolemia – Infections – Pseudomonas spp. Candida – Electrolyte & nutrition (hypermetabolic)
Internal injuries – from fumes (CO, HCN)
– Damages both URT & LRT – Acute respiratory distress syndrome (ARDS)
Hyperthermia
Due to prolonged exposure to ↑ ambient temperatures Heat cramps – exercise w loss of fluids & e-lytes Heat exhaustion – sudden onset of shock, CV system fails to adjust acutely to the hypovolemia, will usually recover spontaneously Heat stroke – temps > 40oC, body core temp ↑’s, peripheral vasodilatation (pooling), ischemia, muscle necrosis (rhabdomyolysis), DIC, confusion, coma, seizures, high mortality rate
Hypothermia
Abnormally low core temperature
– High humidity, wet clothes, vasodilatation (EtOH) all facilitate development of hypothermia
Mild (core temp =) 32-35oC (89-95oF) Moderate 28-32oC (82-89oF) Severe < 28oC (< 82oF) Bradycardia, atrial fibrillation, loss of consciousness
Hypothermia
Frost bite – occurs when the temperature of the extremities falls below freezing At the cellular level hypothermia may lead to cell damage (crystallization of water) Indirect effect of chilling – vasoconstriction, edema, long term may cause atrophy & fibrosis
Radiation Injuries
Sources – cosmic, ultraviolet, elemental (from the earth‟s crust – radon), medical (both diagnostic & therapeutic), industrial, nuclear power plants, weapons Forms:
– Electromagnetic waves – x-rays & gamma rays – High energy neutrons and charged particles – alpha and beta particles, protons
Radiation Injuries
Cellular mechanism of damage (***):
– Direct damage to DNA – Indirect – production of free radicals that can damage membranes, nucleic acids and enzymes
Result may be reversible, may lead to cell death (apoptosis), nuclear changes (pyknosis), cytoplasm changes (membranes, mitochondria and EER)
Radiation Injuries
Rad (radiation absorbed dose) = the amount of energy absorbed per unit mass Chest x-ray - < 0.2 rad Mammography – 0.4 rad Dental (bite) - < 0.4 rad Occupational exposures should not exceed 400 mrem/yr (rem = rad w a quality factor)
Radiation Injuries
Organ Systems effects: Skin: damage occurs over time –
– Erythema (redness) at 2-3 days – Edema 2-3 wks – Blistering/desquamation 4-6 wks – Atrophy & neoplasias months to yrs
Radiation Injuries
Hematopoietic/lymphoid tissues – sensitive
– Lymphocytes in hrs, rebound in wks/mo‟s – Lymph nodes & spleen shrink in size – PMN‟s over 1-2 wks, rebound in 2-3 mo‟s Susceptible to infections ! – Platelets & RBC‟s also , take longer to rebound
Radiation Injuries
Gonads – both sexes – sensitive (sterility) Lungs – sensitive d/t vascularity – pulmonary congestion & edema, ARDS GI tract – v. sensitive – ulcers, strictures, later ‟d risk for cancer Other – blood vessels – endothelial cell injury then fibrosis & narrowing (ischemia)
Total Body Radiation Effects
Lethal range begins about 200 rad and at 700 rad death is certain w/o treatment Acute Radiation Syndromes (3): Hematopoietic – 200-500 rad – GI sx‟s, WBC‟s, infections, sepsis & bleeding GI – 500-1000 rad – severe GI sx‟s, bloody diarrhea, shock, sepsis, death in 10-14 d Cerebral - > 5000 rad – listlessness, drowsiness, seizures, coma, death in 14-36 hrs
Nutritional Diseases
A branch of science that studies the qualitative and quantitative aspects of diet Utilization of components required to maintain health “Adequate diet” should provide CHO‟s, protein & fats for daily metabolic needs Essential amino acids, fats, vitamins & minerals
Malnutrition
Primary – diet is deficient in 1 or more components Secondary – supply is OK, problem w absorption, storage, utilization, excessive losses or drug effects Causes of poor diet – SES, ignorance of needs, fads, acute illnesses (↑‟s BMR), self imposed diet restriction/habits (anorexia/bulimia), malabsorption syndromes (CF, Crohns), genetic diseases
Protein-Energy Malnutrition (PEM)
Common in developing countries
– Up to 25% of children affected – Major cause of morbidity in kids < 5 yrs
Ways to assess nutritional status – body weight (compared to age, sex & height norms), rate of growth (charts) 2 major disorders: Marasmus & Kwashiorkor
Protein-Energy Malnutrition
2 functional protein compartments:
– Somatic – skeletal muscles - more severely affected in marasmus – skinfold thickness – Visceral – liver - more severely affected in kwashiorkor – serum proteins (albumin & transferrin)
When weight falls to < 60% of normal – child has marasmus
Marasmus
Deficiency of caloric intake Catabolize proteins (amino acids) for energy Somatic protein compartment (sk muscle) is depleted. Sub Q fat depleted also.
– Visceral compartment is held in reserve
Extremities are emaciated, head looks out-ofproportion too large
Marasmus
Growth retardation Anemia, multiple vitamin deficiencies
– Bone marrow may be hypoplastic
Immune deficiencies – esp T-cell defects
– Infections are common – Thrush
Serum albumin relatively normal (or sl ‟d) Bradycardia, Body temperature ‟s
Kwashiorkor
Greater deficiency of protein than total calories, more severe than marasmus PEM found in Africa & SE Asia Visceral protein compartment is depleted Low albumin – generalized edema Weight is between 60-80% of normal but this is misleading because of the edema
Infant with Kwashiorkor
Visible edema (puffiness) of the face, hands and legs
From: Robbins Basic Pathology
Kwashiorkor
Skin changes – alternating zones of hyperpigmentation, desquamation & hypopigmentation (flaky paint) Changes in hair texture & color Liver – enlarged & fatty
– Lack of transport proteins
Vitamin and mineral deficiencies Immune system defects – infections Growth retardation
Secondary Forms of PEM
In the US can be found in chronic illness or hospitalized pts Cachexia – a form of PEM seen in cancer patients
– Decreased appetite partly responsible – Increased catabolism – cytokine-mediated (IL-1, IL-6 and TNF)
Vitamin Deficiency
Common in person in lower SES Usually a part of overall malnutrition Fat-soluble (A, D, E, K)
– Require healthy intestinal mucosa, bile & pancreatic secretions for absorption – Are stored in body tissues (compare to watersoluble) – Inflammatory bowel disease (Crohn‟s), Cystic fibrosis, Alcoholic liver disease - ‟d absorption
Vitamin A
1925 found to prevent night blindness 3 biologically active forms – retinol, retinal, and retinoic acid β-carotenes are found in yellow & leafy green veggies, some animal products (liver, fish, eggs, milk) Mainly stored in the liver, reserves for 6-12 months Released w carrier protein – retinol-binding protein
Vitamin A
Functions:
– Maintain vision in reduced light – Augments differentiation of specialized epithelial cells (mucus secreting epithelium) – Enhances immunity to infections (kids, measles)
Vitamin A Deficiency
Deficiency is worldwide – esp 3rd world countries Early sign is impaired night vision Persistent deficiency – Dry eyes (xerosis and xerophthalmia) which can lead to damage to the cornea and total blindness
Vitamin A Deficiency
Epithelia of Respiratory & Urinary tracts are also affected – squamous metaplasia – increases risk for infections and stones Impaired immunity – measles, pneumonia and infectious diarrhea
Vitamin A Toxicity
25,000 IU or more daily
– Over use of vitamin supplements (read labels) – Topical retinoic acid (acne) – this is rare
Acute – N/V, irritability, headache, blurred vision (papilledema symptoms) Chronic – anorexia, hair loss, dry skin (itching), dry mucus membranes, fissured lips, fatigue, weight loss, bone/joint pain
The End !