U.S. Organophosphorus pesticide poisonings- pesticide related marijuana “psychosis”

Full article here: http://www.inchem.org/documents/pims/chemical/pimg001.htm#SectionTitle:7.2%20%20Toxicity

Organophosphorus Pesticides

International Programme on Chemical Safety
Poisons Information Monograph (Group Monograph) G001
Chemical Organophosphorus pesticides

2.1 Main risks and target organs

Organophosphorus pesticides can be absorbed by all
routes, including inhalation, ingestion, and dermal
absorption. The toxicological effects of the
organophosphorus pesticides are almost entirely due to the
inhibition of acetylcholinesterase in the nervous system,
resulting in respiratory, myocardial and neuromuscular
transmission impairment. A few organophosphorus pesticides
have produced the so-called “Intermediate Syndrome” and
delayed neuropathy, the latter apparently unrelated to
acetylcholinesterase inhibition.

The main target organs are the nervous system, respiratory
tract and cardiovascular system.

Degradation products in the environment are not toxic to any
significant extent. Thermal decomposition products may be
harmful by inhalation and skin contamination. Toxicity may

also be due to the effects of solvent vehicles or other
components of formulated pesticides.

…The following UN transportation numbers have
been established for organophosphorus pesticides (UN,
1985):

2783 Organophosphorus pesticides,
solid, toxic, NOS.

2784 Organophosphorus pesticides,
liquid, toxic, flammable, NOS,
freezing point < 61°C, closed cup.

3017 Organophosphorus pesticides,
liquid, toxic, flammable, freezing
point 23°C, closed cup.

3018 Organophosphorus pesticides,
liquid, toxic, NOS.

2.2 Summary of clinical effects

The signs and symptoms of acute organophosphate
poisoning are an expression of the effects caused by excess
acetylcholine (cholinergic syndrome); they may occur in
various combinations and can be manifest at different
times. Signs and symptoms can be divided into three groups:
– muscarinic effect
– nicotinic effect
- central nervous system effect.

According to the degree of the severity of poisoning, the
following signs and symptoms can occur:-

* Mild: anorexia, headache, dizziness, weakness, anxiety,
substernal discomfort, fasciculations of the tongue and
eyelids, miosis, and impairment of visual acuity.

* Moderate: nausea, salivation, bronchorrhoea, lacrimation,
abdominal cramps, diarrhoea, vomiting, sweating,
hypertension or hypotension, and muscular
fasciculations.

* Severe: miosis or mydriasis, non-reactive pupils,
dyspnoea, respiratory depression, pulmonary oedema,
cyanosis, loss of sphincter control, convulsions, coma,
bradycardia or tachycardia, cardiac ischaemia, cardiac
dysrhythmias, hypokalaemia, and hyperglycaemia. Acute
pancreatitis has also occurred. Muscular paralysis may
involve the respiratory muscles.

Some organophosphorus pesticides have caused delayed
peripheral neuropathy.

Intermediate Syndrome: The “Intermediate Syndrome” has been
described. This occurs after initial improvement,
approximately 1 to 8 days after poisoning. Muscle weakness
leading to paralysis and sudden respiratory arrest
occurs.

2.3 Diagnosis

Other relevant laboratory analysis:

Complete blood cell count, serum electrolyte levels, arterial
pH and blood gases, blood glucose, liver function tests,
urine analysis. Investigations may also include ECG and chest
X-ray.

Cholinesterase levels are helpful in diagnosing
organophosphorus pesticide poisoning, but not in managing the
illness. The red cell (acetyl) cholinesterase level is a
more accurate assessment of poisoning. Blood should be drawn
in a heparinised tube before treatment is begun. In cases of
unknown organophosphorus poisoning, the first aspirate or the
formulation of the pesticide if available, may be used to
identify the type of organophosphorus pesticide.

2.4 First-aid measures and management principles

It is important that the chemical be removed as quickly
as possible, as well as atropine to be administered (see
below). Contaminated clothing and contact lenses should be
removed as quickly as possible to prevent further absorption.
If skin contact occurs, the area should be washed carefully
with soap and water. Wash eyes for 15 to 20 minutes with
running water. First-aid personnel should wear rubber or
plastic gloves to avoid contamination, which should be
changed frequently.

In massive overdoses, acute respiratory failure may occur.
It is important to keep the airway open and to prevent
aspiration if nausea and vomiting occur.

There are over 100 organophosphorus compounds
representing a variety of chemical, physical, and
biological properties are presently in commercial
use.

3.4 Hazardous characteristics

The majority of organophosphorus pesticides are liquid
and have different vapour pressures at room temperature. The
compounds used for agricultural purposes are available mainly
as emulsifiable concentrates or wettable powder formulations
for reconstitution as liquid sprays, but also as granules for
soil applications. A limited number are also available as
fogging formulations, smokes, impregnated resin strips for
use indoors, and as animal or human pharmaceutical
preparations.

Environmental risks:

Three routes of entry into water sources are possible. One
is from industrial waste or effluent discharged directly into
water. A second is by seepage from buried toxic wastes into
water supplies. Neither of these should be tolerated, since
prior treatment of the waste with alkali (or acid in cases
such as diazinon), followed by neutralisation, can destroy
the toxic agents.

Thirdly, contamination of running water
directly or from run-off during spraying operations can
occur. No studies on the degradation of organophosphorus
pesticides in running water have been reported. In static
water, in a simulated aquatic environment, there is evidence
that light, suspended particles, and bacteria contribute to
degradation. Thus, the degradation of fenitrothion in lake
water under illumination occurred with a half-life of about 2
days, compared with 50 days in the dark (Greenhalgh et al.,
1980). Furthermore, Drevenkar et al. (1976, as reported in
Gallo & Lawryk, 1991) concluded that although temperature and
pH were major factors controlling the rate of hydrolysis of
dichlorvos in water, large differences in the half-life of
this pesticide in different river waters must be attributed
to microbiological factors.
For guidance on safe disposal, see Section 12.2.

4.1.2 Description

Organophosphorus pesticides are used to control
insect vectors which are found in food and commercial
crops, and infestations in domestic and commercial
buildings, and in man or domestic animals.

Di-isopropanyl fluorophosphate (DFP) is used as an
ophthalmic cholinesterase inhibitor to treat
glaucoma.

4.2 High risk circumstances of poisoning

…Occupational exposure among adult farm workers and secondary
accidental exposure to their families can occur.

…Exposure of the general population through the consumption of
foodstuffs treated incorrectly with pesticides or harvested
prematurely before residues have declined to acceptable
levels from contact with treated areas, or from domestic use
has been reported. Accidental poisonings can also occur
through failure to observe the safe re-entry time after
application.

4.3 Occupationally exposed populations

- Factory workers involved in synthesizing
pesticides.
– Workers involved in formulating and dispensing
pesticides.
- Agricultural spray workers.
- Crop harvesters during disease vector control periods.

- Public-health workers involved in vector control.
– Health workers not following the correct procedures when
handling poisoned patients, especially when ventilatory
support is needed.

5. ROUTES OF EXPOSURE

5.2 Inhalation

The majority of organophosphorus pesticides are liquids
that have different vapour pressures at room temperature
(e.g., dichlorvos is much more volatile than parathion);
thus, hazards due to inhalation of vapour vary from compound
to compound. Respiratory exposure is greater when dusts are
applied than when dilute sprays are used. However, aerosols
of concentrated pesticide may be an even greater hazard
(WHO,1986).

5.3 Dermal

Many accidental acute poisonings have occurred after
spillage of a pesticide on skin and clothing. The extent of
uptake will depend on persistence time (related to
volatility, clothing, coverage, and thoroughness of washing
after exposure), and also on the presence of solvents and
emulsifiers that may facilitate uptake. Powder formulations
also have a potential for skin absorption (Wolfe et
al.,1978).

Skin absorption is somewhat greater at high temperatures and
may be much greater in the presence of dermatitis, thus,
leading to serious poisoning after an exposure that would
ordinarily cause no effects (Gallo & Lawryk, 1991).

5.4 Eye

Exposure to vapours, dusts, or aerosols can cause local
effects on the smooth muscles of the eyes. Systemic
poisoning may follow.

6. KINETICS

6.1 Absorption by route of exposure

Organophosphorus pesticides are absorbed by the skin as
well as by the respiratory and gastrointestinal tracts.

Oral exposure:
When 32P-dimethoate was given orally to volunteers, it was
absorbed and excreted rapidly: 76 to 100% of the
radioactivity appeared in the urine in 24 hours (Edson et
al., 1967).

Inhalation exposure:
Exposure by respiratory and dermal routes were compared in
workers spraying parathion, who either breathed a pure air
supply but did not wear protective clothing, or who wore
total protective clothing but did not have any respiratory
protection (Durham et al., 1972).

6.3 Biological half-life by route of exposure

It is possible to determine the rate of disposal of
metabolites and thereby to estimate an approximate half-life
of the pesticide in the body.
(Lyon et al., 1987).

A few organophosphorus pesticides, however, are lipophilic
and may remain in the body for many days or weeks (see
section 6.2). For example, leptophos tends to persist in the
fat of hens, and pharmacokinetic studies using radiolabelled
leptophos showed an elimination half-life of 17 days
(Abou-Donia & Graham, 1978).

7. PHARMACOLOGY AND TOXICOLOGY

7.2 Toxicity

Most organophosphorus pesticides are
highly toxic. The level of toxicity
(described below) ranges from an estimated
human oral LD of < 5 mg/kg to 0.5 to 5
g/kg(Gosselin et al., 1984).

…The estimated fatal dose of diazinon in
humans is 25 g by oral ingestion (Baselt,
1982).
…The mean fatal dose of malathion in humans is
estimated to be 60 g (Baselt, 1982). The
mean lethal oral dose of malathion in an
untreated adult may be as low as 250 mg/kg
(Gosselin et al., 1984).

7.2.1.2 Children

Children have died after ingesting
only 2 mg of parathion equal to a dose of
about 0.1 mg/kg. Young animals are more
susceptible than adults of the same species,
and the same may be true of children
(Gosselin et al., 1984).

9. CLINICAL EFFECTS

9.1 Acute poisoning

9.1.1 Ingestion

The clinical picture of organophosphorus
pesticide poisoning results from accumulation of
acetylcholine at nerve endings. Signs and symptoms can
be divided into three groups: muscarinic,
nicotinic,and central nervous system (CNS) effects
(see table 9.1.1). Some of these effects may be more
prominent than others or may occur first.

Table 9.1.1 Clinical Effects of Organophosphorus
Pesticide Poisoning

MUSCARINIC EFFECTS
– increased bronchial secretion, excessive sweating,
salivation, and lachrymation
– pinpoint pupils, bronchoconstriction, abdominal
cramps (vomiting and diarrhoea)
– bradycardia

NICOTINIC EFFECTS
– fasciculation of muscles. In more severe cases,
paralysis of diaphragm and respiratory muscles
– tachycardia and elevation of blood pressure

CENTRAL NERVOUS SYSTEM EFFECTS
– headache, dizziness, restlessness, and anxiety
– mental confusion, convulsions and coma
– depression of the respiratory centre and vasomotor
centre
(Reference: WHO, 1986)

Systemic effects are, in general, similar,
irrespective of the route of absorption, but the
sequence and times may differ. Respiratory and ocular
symptoms are expected to appear first after exposure
to airborne organophosphates. Gastrointestinal
symptoms and localised sweating are likely to appear
after oral and dermal exposure, respectively.

Following ingestion, the onset of symptoms is usually
rapid, within a few minutes to 1 or 3 hours. Clinical
effects vary according to the amount ingested (see
table 9.1.1). All of the symptoms and signs may occur
in various combinations and can be manifest at
different times, ranging from a few minutes to many
hours, depending on the chemical, dose, and route of
exposure.

Mild poisoning may include muscarinic and
nicotinic signs and symptoms only. Severe cases
always show CNS involvement; the clinical picture is
dominated by respiratory failure, sometimes leading to
pulmonary oedema, due to the combination of the
effects of all three groups.

***Note from Anna:  If you grow marijuana organically the only signs of MMJ-related “psychosis” you’ll be worrying about will be from the moronic politicians, dispensary owners, and doctors who cannot figure out how to educate themselves about MMJ. Big pharmaceutical companies grow with poisonous pesticides, you don’t have to.

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