Chemicals and Society

 

 

The 20^th century has seen the birth of three Ages, each with profound social implications.  These have been called the Nuclear Age, the Electronic Age and the Chemical Age.  The latter is the oldest (beginning ca. 1930), and although its impact has been less dramatic than the other two, its consequences have more thoroughly and deeply permeated our day-to-day lives.  Our local grocery, hardware, garden and drug stores carry an impressive array of commonly used chemical “tools”, such as detergents, adhesives, lubricants, fabrics, pesticides, pharmaceutical drugs, vitamins and a multitude of fabricated plastic items.  Industrial applications of chemical tools include explosives, heat-transfer gases and liquids, specialized coatings, fire retardants and high-performance plastic components.

Despite our widespread use of chemical tools, indeed some might say because of our reliance on them, large numbers of people fear exposure to these materials, and have deep concerns regarding the use, storage and disposal of chemicals.  Paradoxically, we find our desires for more abundant consumer goods, energy and personal mobility in conflict with maintenance of a healthful environment.  To be sure, environmental degradation, with accompanying threats to health and disruption of ecosystems, is not a new phenomenon.  From the earliest recorded history, human disturbance of the environment by deforestation, air pollution from cooking and heating fires, and careless sewage and waste disposal has been noted.  Today, as global populations grow and per capita energy use and material consumption increases, pollution problems are exacerbated, and previously unnoticed secondary effects manifest themselves.

It must be emphasized that effective strategies for safeguarding our environment require knowledge and understanding.  To this end, we must be able to answer the following questions:

·        What potentially undesirable substances are present in our air, water, soil and food?

·        Where did these substances come from?

·        What options, alternative products and processes are available to reduce or eliminate known problems?

·        How does the degree of hazard depend on the extent of exposure to a given substance, and how shall we choose among various corrective options?

The first of these questions requires chemical analysis, and for this purpose the spectroscopic methods described in chapter 2 and 9 in the textbook are particularly useful.  Answers to the second question usually involve collaborative investigations by analytical chemists together with biologists, meteorologists, volcanologists, oceanographers and other scientists.  The development of options, as noted in the third question, calls upon our full range of chemical understanding, and often obliges us to make controversial choices.  For example, the world mortality rate due to malaria was drastically reduced (>95%) in the 1950s by widespread application of the insecticide, DDT.  Because of this chemical’s environmental persistence and toxicity to certain birds and crustaceans, production of DDT was effectively terminated ca. 1964.  Third world malaria cases immediated spiraled, reaching over 250 million in 1990.  Cheap, effective and environmentally friendly alternatives to DDT are needed, but are not necessarily easy to find.  The fourth question is addressed by physicians, toxicologists and epidemiologists.  A substantial body of knowledge has accumulated on this subject, but there is also considerable public confusion surrounding it.  We all seek to minimize risk: but we must recognize that society cannot afford to pay the excessive costs of eliminating all risk, a virtually impossible goal.

As with any other kind of tool, chemicals must be handled correctly, with proper care and precaution.  Although chemicals vary in the hazards they present, it is generally wise to treat all chemicals as though they are potentially dangerous.  Among the recognized hazardous properties of chemicals are:  explosiveness, flammability, corrosiveness, irritation, sensitivity, toxicity and radioactivity.  One of the most useful sources of information about chemical hazards is the material safety data sheet (MSDS).  A typical MSDS is attached.  Note that you can by pure naphthalene from supermarkets.

Of all the hazardous properties noted above, toxicity seems to constitute the greatest concern in the minds of the public.  Contrary to popular belief, the fact that a substance is toxic does not mean it will always kill people or animals exposed to it.  Virtually all substances are lethal if taken in sufficient amount.  As noted by the Swiss physician Paracelsus, it is the dose that makes the poison.  Thus, 1.5 g of arsenic trioxide will kill a 180 pound person, 2 milligrams will not.  Small amounts of vitamin D (ca. 10 micrograms per day) are necessary for good health, but in larger amounts it is more toxic than arsenic compounds.  Some qualitative and somewhat arbitrary levels of toxicity are listed in Table 1.  Most of the poisons we are familiar with are acute toxins, that is they cause immediate death in sufficient dose.  The relative toxicity of such substances is roughly indicated by an LD₅₀ dosage, the amount of a chemical (adjusted for subject body weight) that kills one half of a large group of test animals.  Some examples of LD₅₀’s for common substances are given in Table 2.  For highly toxic materials the LD₅₀ is usually given as mg per kg (Table 3).  Note that LD₅₀’s vary markedly with the animal species used, and the way in which the test substance is administered.  Also the toxicity of a given substance has no relationship to whether it is synthetic (manufactured) or natural.  Finally, acute toxicity is only one of several toxic characteristics that should be considered, others are described in Table 4.

 

Table 1.  Levels of toxicity (death after acute poisoning).

Toxicity Class	Lethal Dose (oral or intravenous)	Examples of chemicals
Biotoxins	Much less than 10 mg/kg	Ricin (from castor oil plant), botulinum toxin
Supertoxic	10 mg/kg -1 mg/kg	Nerve agents, atropine (from deadly nightshade)
Highly toxic	1-50 mg/kg	Some organophosphorus insectidices, sodium cyanide, vitamin D
Moderately toxic	50-500 mg/kg	Organophosphorus and organichlorine insecticides, barbiturates
Slightly toxic	0.5-5 g/kg	Aspirin, many commercial ‘solvents’
Hardly toxic	> 5 g/kg	Vitamin B1, glucose

 

Table 2.  LD₅₀’s of familiar substances.

Substance	Animal	LD50 (g/kg unless noted)
Acetaminophen	Mice	0.34
Acetic acid	Rats	3.53
Arsenic trioxide (murder story poison)	Rats	0.015
Aspirin	Mice, rats	1.5
BHA (antioxidant food additive)	Mice	2
BHT (antioxidant food additive)	Mice	1
Caffeine	Mice	0.13
Citric acid	Rats (abdominal injection)	0.98
Ethyl alcohol	Rats	13 mL/kg
Glucose	Rabbits (intravenous)	35
Niacin (vitamin B4)	Rats (injection under skin)	5
Nicotine	Mice	0.23
Sodium chloride	Rats	3.75
Thiamine hydrochloride (vitamin B1)	Mice	8.2
Trisodium phosphate (food additive)	Rats	7.4

 

 

Table 3.  Approximate LD₅₀’s of the most lethal poisons (Naturally occurring substances in bold).

Substance	LD50 (mg/kg in mice or rats unless noted)
Botulinum toxin A	0.00000003
Tetanus toxin A	0.000005
Diptheria toxin	0.0003
TCDD	0.03
Muscarine	0.2
Bufotoxin	0.4 (cats)
Sarin	0.4
Strychnine	0.5
Soman	0.6
Tabun	0.6
Tubocurarine chloride	0.7
Rotenone	3
Isoflurophate	4
Parathion	4  (female rats) 13 (male rats)
Aflatoxin B1	10
Sodium cyanide	15
Solanine	42

 

Table 4.  Summary of test methods for the toxicity of chemicals.

Test	Procedure
Acute lethality (LD50)	Treat animals with a range of doses, and count number of dead after a set time (usually 24 h).  Make pathological examinations of dead and survivors. Usually simple dosing route (e.g. intravenous)
Whole-animal monitoring	Lightly anaesthetize animal, then apply instruments to measure physiological parameters, such as respiration rate, heart rate, arterial and vnous blood pressures, electrical activity of brain and heart, etc.  Increase dose of chemical very slowly (instraveneous infusion is preferred and follow changes in the parameters being measured.
Chronic toxicity	Repeated treatment of animals with sublethal doses.  Do pathological examination at set times (1 month, 6 months, 2 years, for example) and note all unusual features. Route of dosing must reflect practical risk (e.g. oral for foodstuffs, inhalation for vapors).
Carcinogenicity	As for chronic toxicity, paying particular attention to tumors and incipient changes in tissues. Use cofactors to increase artificially the production of cancers.
Mutagenicity	Test ability of chemical to induce growth in a microorganism that has been inhibited by a genetic manipulation (Ames test). Pre-incubate chemical with enzymes from liver, to see if it is readily transformed in the body to a mutagen. Check for any gross effects on the structure of nucleic acids in chromosomes by microscopy.
Teratogenicity	Treat pregnant mother with chemical at appropriate doses by the relevant route.  Choose period of pregnancy most sensitive to chemicals (first third).  Count number of aborted fetuses, stillbirths and survivors.  Make pathological examination of all fetuses.