Вы находитесь на странице: 1из 7

PATHOLOGY AGRICULTURAL HAZARDS.

Section 2B7 (2016-2017)

Farmworkers are exposed to numerous safety, health, environmental, biological, and


respiratory hazards. These include vehicle rollovers, heat exposure, falls, musculoskeletal
injuries, hazardous equipment, grain bins, unsanitary conditions, pesticides, and many
others.

BIOLOGIC
Zoonosis
a. Common sources: Anthrax (contact), Brucellosis (contact), Campylobacter and cryptosporidium
(ingestion of contaminated animal), leptospirosis (contact with contaminated water), psittacosis
(inhalation of fecal matter), rabies (bites from infected animals)
b. Diseases associated: Infectious diarrhea, Influenza, pneumonia
c. Usual type of exposure/mode of entry: handling of infectious animals (contact, ingestion,
inhalation)
d. Mechanism of toxicity: bacterial toxins
e. Early and delayed effects of acute and chronic exposure
a. Diarrhea
b. Neurologic problems (rabies)
f. Overview management of acute exposure
a. Palliative care: fluid replacement?
g. Prevention/limiting of delayed effects
a. Early detection
b. Vaccination (animal and human)
c. Maintenance of safe water supplies
d. Proper disposal or human and animal wastes/ sanitation
e. Proper food handling
f. Use of PPE
g. Avoid contact of infected animals: Handwashing
Microorganisms
A. Meliodosis
a. Source: Burkholderia pseudomallei
b. Associated disease: Meliodosis (Vietnamese Time bomb)
c. Usual type of exposure/mode of entry: contact, inhalation, ingestion of contaminated water/soil
d. Mechanism of toxicity
e. Early and delayed effects of acute and chronic exposure
a. Acute exposure
i. Localized infection: Localized pain or swelling, fever, ulceration, abscess
formation
ii. Pulmonary infection: cough, high grade fever, headache, anorexia
iii. Bloodstream infection: fever, disorientation, headache, abdominal discomfort,
joint pain, resp distress,
b. Chronic exposure
i. Disseminated infection: stomach, chest pain, myalgia, arthralgia, seizures, fever,
weight loss, headache
f. Overview management of acute exposure
a. Treatment: Antibiotics- Ceftazidine, Meropenem, Trimethoprim-sulfamethoxazole,
doxycycline
g. Prevention/limiting of delayed effects
a. Prevent acquisition: wear boots/appropriate footwear
b. Avoid contact with contaminated soil or standing water.
B. Tetanus
a. Source: Clostridium tetani
b. Associated disease: Tetanus
c. Usual type of exposure/mode of entry: contact through breaks in the skin
d. Mechanism of toxicity: tetanus toxin
e. Early and delayed effects of acute and chronic exposure
i. Acute exposure
1. Early effects
a. Muscle spams (jaw muscle) lock jaw
b. Headache
c. Jaw cramping
d. Myalgia and body stiffness
e. Jerking or staring
f. Seizures
g. Difficulty in swallowing
h. Fever
i. Sweating
j. Hypertension
k. tachycardia
2. Delayed effects
a. Laryngospasm
b. Fractures
c. Pulmonary embolism
d. Pneumonia
e. Resp distress
ii. Chronic exposure: fast onset, signs and symptoms are fatal even in early
exposure
f. Overview management of acute exposure
i. Tetanus antitoxin: Tetanus immunoglobulin, tetanus toxoid
ii. Palliative treatment: Phenobarbital, Chlorpromazine (spasms)
g. Prevention/limiting of delayed effects
i. Palliative care

C. Glanders
a. Source: Burkholderia mallei
b. Associated disease: Glanders
c. Usual type of exposure/mode of entry: contact thru cuts skin abrasions or exposed
mucosa, inhalation aerosols or dust
d. Mechanism of toxicity
e. Early and delayed effects of acute and chronic exposure
i. Acute exposure
1. Fever
2. Chills
3. Headache
4. Sweating
5. Myalgia
6. Chest pain
7. Chest tightness
8. Nasal discharge
9. Light sensitivity with excessive tearing of eyes
ii. Chronic exposure
1. Disseminated infection: stomach, chest pain, myalgia, arthralgia,
seizures, fever, weight loss, headache
f. Overview management of acute exposure
g. Prevention/limiting of delayed effects
i. Early identification and elimination of infection in the animal population

Parasites
A. Hookworm Infection
a. Common sources: Hookworm
b. Diseases associated: Hookworm infection, cutaneous larvae migrans
c. Usual type of exposure/mode of entry: contact through walking barefoot
d. Mechanism of toxicity: parasitism, release of anticoagulant (bleeding), hooks to intestinal wall
e. Early and delayed effects of acute and chronic exposure
a. Early effects
i. Blood loss
ii. Anemia
iii. Protein deficiency
b. Delayed effects
i. Growth and mental retardation
f. Overview management of acute exposure
a. Antihelminthic drugs: Mebendazole, Albendazole
g. Prevention/limiting of delayed effects
a. Avoid walking barefoot
b. Effective sewage disposal systems

B. Vector-borne infections and other parasitic infections


a. Common sources:
b. Diseases associated: Dengue, Trypanosoma, Leishmaniasis, Schistosomiasis, Malaria, Ascariasis,
Filariasis, Tricuriasis, Ascariasis, etc.
c. Usual type of exposure/mode of entry: Vector (flies), ingestion, contact
d. Mechanism of toxicity: parasitism
e. Early and delayed effects of acute and chronic exposure
i. Depends on the organism involved
f. Overview management of acute exposure
i. Antihelminthic drugs: Mebendazole, albendazole
ii. Antimalarial drugs
iii. Palliative (dengue): platelet transfusion or fluid replacement
g. Prevention/limiting of delayed effects
i. Proper irrigation system
ii. Prophylaxis treatment for parasitis
iii. Elimination of breeding sites
iv. Use PPE, mosquito netting
CHEMICAL: PESTICIDES
Herbicides and Rodenticides
A. Common sources: Insecticides, herbicides, fungicides, rodenticides, fumigant, insect repellants
B. Diseases associated
a. Upper and respiratory tract infections
b. Asthma
c. Folliculitis- herbicides
d. Acneiform dermatosis- herbicides
e. Pulmonary fibrosis
f. Bleeding (Warfarin-based)- herbicides
C. Usual type of exposure/mode of entry:
a. Dermal and Inhalation (Usual)
b. Transplacental and Ingestion (Unusual)
D. Mechanism of toxicity
a. Irritation
b. Allergic sensitization (Histamine-induced)
E. Early and delayed effects of acute and chronic exposure
a. Acute Exposure
i. Dermal irritation (blistering, ulcerations, discoloring of fingernails)
ii. Ocular irritation
iii. GIT: Vomiting, Diarrhea, Abdominal Pain
b. Chronic Exposure
i. Cancer: Leukemia, non-Hodgkins Lymphoma, Multiple myeloma, lung cancer
ii. Reproductive: fertility, decrease sexual function
iii. Endocrine: agent and its metabolites act like hormones
iv. Neurotoxicity
v. Liver disease
vi. Thyroid diseases
vii. Allergic dermatitis
F. Mechanism of elimination of toxicity
G. Overview management of acute exposure
a. Airway management
b. Antidote: Atropine
c. Charcoal administration
H. Prevention/limiting of delayed effects
a. Early management
b. Prevent from acquiring: Avoid use, PPE (gloves, long sleeve clothes)

Biopersistence
It is the ability of a fibre (a particle with a length to width ratio of at least 3:1 which can reach the deepest
parts of the lungs) to remain in the lung. It is a function of the solubility of the fibre in the lung, and the
biological ability of the lung to clear the fibre from the lung.
a. Common sources: dusts?, silica, asbestos?
b. Diseases associated: Lung cancer (silica asbestos), COPD (grain dust, coal dust), Pulmonary
Fibrosis (silica, asbestos)
c. Usual type of exposure/mode of entry: Inhalation
d. Mechanism of toxicity: formation of reactive oxygen species
e. Early and delayed effects of acute and chronic exposure
a. Acute exposure
i. Early effects
ii. Delayed effects
b. Chronic exposure
f. Overview management of acute exposure
g. Prevention/limiting of delayed effects
Inhalability: ratio of the particle (fibre) concentration in the inhaled air to that in the
ambient air. (The inhalable fraction of an aerosol consists of particles than can enter
nose or mouth upon inhalation.)
Respirability: ratio of airborne particles (fibres) penetrating to the alveolar region of
the lung to that in the ambient air

Organochlorines (include Bioaccumulation specifically these agents: DDT, dieldrin, Aldrin,


polychlorinated biphenyls which are mostly hydrophobic, can cause toxicity in the body since they are
not easily excreted)
These are synthetic lipophilic products that resist degradation. Important organochlorines used as
pesticides include DDT or dichlorodiphenyltrichloroethane, lindane, Aldrin and dieldrin. Nonpesticide
polychlorinated biphenyls.
Bioaccumulation means an increase in the concentration of a chemical in a biological organism over time,
compared to the chemical's concentration in the environment. Compounds accumulate in living things any
time they are taken up and stored faster than they are broken down (metabolized) or excreted. The
concentration of a chemical (foreign to an organism) in an organism becomes higher than its
concentration in the air or water around the organism.
a. Common sources: see stated above artificial products
b. Diseases associated: Breast Cancer, Parkinsons disease, neurotoxic, endocrine diseases,
immunotoxic
c. Usual type of exposure/mode of entry: Contact, Inhalation, Oral (GIT)
d. Mechanism of toxicity: Inhibition of neurotransmission (GABA inhibition and alteration in
Calcium homeostasis), Hydrophobic and lipophilicity increases binding capacity to fats causing
toxicity especially during increased energy demand (lipolysis)
e. Early and delayed effects of acute and chronic exposure
a. Acute exposure
i. Early effects
1. Sensory and motor disturbances
2. Headache
3. Mental confusion
4. Dizziness
ii. Delayed effects
1. Coma
2. Respiratory depression
b. Chronic exposure
i. Antiestrogenic activity (dec. estrogen)
ii. Antiandrogenic activity (dec. androgen)
f. Overview management of acute exposure
a. Airway management
b. Antidote: Atropine
c. Charcoal administration
g. Prevention/limiting of delayed effects
a. Early management
b. Prevent from acquiring: Avoid use, PPE (gloves, long sleeve clothes)

Organophosphates
a. Common sources: pesticide
b. Diseases associated: Organophosphate poisoning
c. Usual type of exposure/mode of entry: Contact (skin absorption)
d. Mechanism of toxicity: inhibition of cholinesterase activity
e. Early and delayed effects of acute and chronic exposure
a. Acute Exposure
i. Early effects
1. Cholinergic crisis (high acetylcholine)
2. Flu-like: headache, excess salivation, nausea
ii. Delayed effects
1. Respiratory distress
2. Death
b. Chronic exposure
f. Overview management of acute exposure
a. Airway management
b. Antidote: Atropine
c. Charcoal administration
g. Prevention/limiting of delayed effects
a. Early management
b. Prevent from acquiring: Avoid use, PPE (gloves, long sleeve clothes)

Carbamates
a. Common sources: pesiticide
b. Diseases associated: Carbamate Poisoning
c. Usual type of exposure/mode of entry: Contact (skin absorption)
d. Mechanism of toxicity: Inhibition of cholinesterase activity
e. Early and delayed effects of acute and chronic exposure
a. Acute Exposure
i. Early effects
1. Cholinergic crisis (high acetylcholine)
2. Flu-like: headache, excess salivation, nausea
ii. Delayed effects
1. Respiratory distress
2. Death
b. Chronic Exposure
f. Overview management of acute exposure
a. Airway management
b. Antidote: Atropine
c. Charcoal administration
g. Prevention/limiting of delayed effects
a. Early management
b. Prevent from acquiring: Avoid use, PPE (gloves, long sleeve clothes)

*include CaO/Lime, Ammonia, Hydrogen sulfide, hydrogen peroxide, methane, coliforms

PHYSICAL
a. Common sources
b. Usual type of exposure/mode of entry
c. Mechanism of toxicity
d. Early and delayed effects of acute and chronic exposure
e. Overview management of acute exposure
f. Prevention/limiting of delayed effects

Вам также может понравиться