Noxious organism control agents
Chemical warfare: adapted for your dog...
Many of today's synthetic insecticides (biocides: “noxious organism control agents”) are powerful poisons that had their origin in the development of chemical warfare agents (neurotoxins), and are classified as carcinogens (cancer causing) by the Environmental Protection Agency (EPA).
Organophosphates (OPs) and carbamates are common synthetic pesticides (produced by chemical or biochemical synthesis) found in flea & tick killers. Both are nerve-paralyzing agents capable of causing convulsions, nausea and respiratory arrest: not only in the insects they are intended to obliterate, but in the host animal (your dog) as well. Research spanning decades classifies many as mutagens (causing cellular or genetic damage), as well as hormone and immune system disrupters.
But don't touch...
The peak flea and tick season invariably results in innumerable cases of pesticide-related poisoning of not only the targeted dog, but often also, children and other pets who touch them.
Paradoxically, application instructions on many products direct you to vigorously rub powders deep into your dog’s coat; or, to wet, sponge-soak or even submerge an insect-afflicted dog thoroughly with a spray or concentrated bottled formula (a so-called “flea dip”)… while in parallel, strictly warning of the hazards to humans or other non-target animals. Among the cautionary language are advice for consumers to “wear protective eyewear,” wash themselves thoroughly after handling the product (that they pour on the dog's back), and to remove or wash clothing that comes into contact with the treatment. One must work to prevent the dog from shake-spraying the toxin throughout the house before it dries. Once finished applying, the admonishment continues: “do not pet” your dog for 24 hours, keep same-household dogs separated during that period; and concluding with: “Do not contaminate water, food or feed by storage and disposal.” After all... it isn't the simple century carbolic-acid based "sheep dip" farmers used in the 19th century... it's “better living through chemistry.”
Insecticidal powders (including dispersions from flea or tick collars) can be inhaled or licked off by your dog; and especially in liquid or topical formulations, these chemicals are intended to be absorbed through his skin and then attach to blood plasma: and thereby circulate through his entire body. This systemic (see below) mode of application may, depending upon factors of individual sensitivity,
set the stage for a myriad of adverse effects, including genetic damage and
vital organ failure.
Aside from immediate toxicity, many researchers link the rise in cancer seen in companion animals and residual chemical persistence in the environment to the use of chemical pesticides against fleas and ticks.
For that reason, even in the midst of an insect invasion, it's important not to let the urgency of your need to get rid of the pests override the risk factors for your dog, other pets, and the household; nor, to be complacent about the pervasive environmental issues raised by use of these products, which the National Resources Defense Council describes as “rash and unnecessary.”
The Mythology of “Safety”:
How We Use the Benefit vs. Risk Standard
It is unwise to assume that because a product is available at
the grocery store,
that it has been tested
Nor should you take this assumption regarding a “professional” pest control applicator, or even products recommended by your veterinarian.
The 1947 law regulating pesticides—the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) ( [P.L. 75-717] 7 USC § 136 et.seq.)—is based on a benefit-risk standard, and does not use safety as the fundamental basis for permitting a pesticide on the market. This allows pesticides to be used even if they pose hazards to humans and the environment, so long as the benefits outweigh the hazards: any health or environmental threat can be acceptable if the estimated economic benefits
FIFRA has been amended many times, most recently through the 1996 Food Quality Protection Act; however, imposed deadlines have not been met, some registered pesticides do not meet current testing standards, and the EPA has little information about the cumulative impact of multiple organophosphates or of other similarly functioning chemicals. In 2018, ongoing reorganization and broad budget cuts designed to deconstruct the agency and loosen environmental and health standards have amplified public concern.
“Active” vs. “Inert” Ingredients: What's the Difference?
To evaluate the risks associated with any of these products, it is important to understand that flea & tick pesticides are made up of more than one chemical: composed of “active” ingredient(s), whose identity must be listed on the label (percentage by weight); and “inert” ingredients which do not have to be disclosed.
FIFRA allows manufacturers confidentiality on issues they claim would otherwise make them vulnerable to market competition. As such, “inert” ingredients became protected by industry as “trade secrets.”
60 years on, however, it is clear that the act protects commerce, yet supersedes the public’s right to know to about many chemical formulations, and thus impedes the consumer’s awareness of health hazards resulting from exposure to un-named chemicals. Without full disclosure—not even a veterinarian is able to acquire this information—the consumer is unable to make educated decisions as to which chemicals to avoid. Contemplating concepts of consumer rights and manufacturer liability exposure, it is troubling to remember that legally, dogs are considered “property,” and therefore limited in value to “cost of purchase.”
While the word “inert” suggests benign effect (and likely connotes “safety” to the consumer), this is misleading, because these undisclosed ingredients may not be biologically, chemically, or toxicologically inactive: legally, “inert” merely means those substances that are not the “active” (registered) ingredient.
From a marketing perspective, consumers may feel comforted by the concept that a product contains only a minuscule amount of an “active” ingredient, and up to 99.9 percent “inert” ingredients, suggesting they are inactive: probably only carriers, conditioners, (excipients) etc. (in fact, many manufacturers simply substitute the term “inactive” for that reason). The understanding should be different, however: because testing required for EPA registration is rigorous only for the “active” ingredients, whose toxicological profiles must be disclosed on inserts and packaging. Not so, for the “inert” ingredients, generally tested in short-term studies for acute (immediate) toxicity only. Moreover, the cumulative and synergistic effects of these chemicals (the interaction of chemicals that when combined produce a total effect that is greater than the sum of the individual chemicals), are not required to be tested for safety.
In actuality, many “inert” ingredients are as toxic, or more toxic, than the registered “active” ingredients. In 1987, EPA “requested” registrants of pesticide products to voluntarily substitute the term “other ingredients” in lieu of the term “inert ingredients” on the label. According to the EPA’s Review of 2008 Incident Reports for Spot-on Insecticides: “These ingredients may have been responsible for a number of the (adverse) incidents as some have toxic properties…” In the current marketplace, neither the consumer or his veterinarian has means to gain knowledge about what these ingredients might be, and expectations about safety must be conditioned
on that basis.
So... What’s the
Pri¢e of $afety?
LD50 and LC50 Poison Testing
US consumers expect that products on store shelves have been vetted (registered) by the EPA’s Pesticide Division for safety before marketing. But how (or if?) is this accomplished?
LABORATORY “TOXICOLOGICAL” (POISON) TESTING
is done on healthy “domestic animals” (mice, rats, dogs and cats) to confirm the median lethal dose or LD50: the dose at which the product (toxicant) would poison/kill 50% of a of a test population after a specified test duration, in order to determine acute (not chronic) effects.
Generally without anesthesia or other medication (under the assumption that “relief” from pain or nausea/gastrointestinal distress would alter test results), animals are force-fed (oral LD50), injected into tissues or “body cavities” (injectable LD50), wiped (dermal LD50), or clamped with masks (inhalation LD50).
Similar measures include LC50 (Lethal Concentration, 50%) or LCt50 (Lethal Concentration & Time, 50%), also known as Haber's Law: a mathematical statement of the relationship between the concentration of a poisonous gas and how long the gas must be breathed to produce death, or other toxic effect.
The heavily criticized LD process may substitute the modernized “Up and Down Procedure,” in which fewer test animals are dosed singly and the dosage of subsequent animals is increased or decreased based on the survival of the
A “clinical/health assessment” (a checklist designed to quantify and standardize symptoms) using a “rubric” scoring guide is used to determine the highest experimental point that is without adverse effect, called the No Observed Adverse Effect Level (NOAEL). NOAEL is used to support establishing a dose-response relationship as part of risk assessment for regulatory approval, and as such, serves as the basis for EPA “safety” level, or “reference dose.” The results are mathematically extrapolated to make judgments regarding general consumer application, and adjusted for weight of the dog, although the very generalized nature of the process may make that figure unreliable. During and following the study, certain surviving animals are killed in order to review identifiable system damage to vital organs (lungs, kidneys, etc.).
What are observable "clinical symptoms"?
It's important to understand that veterinary professionals (as well as insurance companies and legal experts) identify and define adverse effect according to “clinical symptoms” that are “observable.” That is: signs that are strictly visible (evident because they can be seen) to the study team, or, otherwise identified in some other tangential way. Thus, it is only “acute” adverse reaction that would be noted during the research process. (See: Pharmacovigilance: What is “Adverse Drug Event” Reporting?, below).
This imbedded limit on “scientific” definition constrains the framework of how veterinary drugs are evaluated, submitted for regulatory approval, and marketed: since “sub-acute” (systemic, or internal) reactions are not identified as relevant in any way. Although the ability of a dog to tolerate a powerful insecticide or drug depends on his total immune response—which can be influenced by a myriad of factors, including heredity, general health, as well as environmental, food, or stress pressures—that is only relevant to the extent that an adverse reaction would manifest both swiftly and visibly.
ACUTE and RAPID ONSET DISEASE TESTS
Skin “corrosivity” and inflammation reactions, the eye-irritancy “Draize” test, and nervous system effects can reveal issues in a comparatively short time period. These studies are conducted for 3 to 26-week intervals, using exaggerated dosages to compensate for the short testing periods. While health effects resulting from high doses of the chemicals are relevant, they do not reveal possible chronic effects (examples: cancer, developmental or reproductive damage, DNA damage, immune system suppression) that may take months or years to manifest. Commonly also unaccounted for, is individual, sex, and breed sensitivity: a minimal “impact dose” for one animal could be lethal to another, even adjusted for weight; small and other so-called high-strung breeds or females are particularly susceptible to neurotoxin adverse side-effects.
Long-term testing is not generally undertaken, as it is ordinarily not required for regulatory approval, and as such, the cumulative effect of pesticide use over the lifetime of the dog is simply not known from product development research. Further, the EPA does not require testing for the synergistic effect of the combined influence of chemical exposure and outdoor environments (and those are not replicable in the laboratory). In the final analysis, we are failing to acknowledge and question that, essentially, it is the dog himself who becomes a living chemical research vessel of insecticide over his lifetime.
It is the dog himself who becomes a living chemical research vessel over his lifetime
Remember that pursuant to FIFRA, the EPA registers pesticides on a COST-versus-BENEFIT BASIS: weighing health and environmental concerns against the economic gain/benefit to the manufacturer and the end user of the product. As such, this “risk-benefit balancing analysis” represents an especially significant relationship to “over the counter” (OTC) treatments, which may cost less than half of a veterinary-
Currently, no pre-market clinical trials (studies on pets in a “real world” environment, before the product goes on the market) are required for EPA or FDA approval, and the confined, short-term tests are often only on one breed of dog, limiting the veracity of predicted effects across a broader population of users. According to the National Research Defense Council, the EPA’s “risk assessments have been handicapped by flawed and inconsistent assumptions that understate the risk from pet products,” and which do not adequately account for environmental issues of pesticide bio-accumulation, bio-concentration and pesticide bio-magnification. In fact, in the summary of meetings between the EPA and manufacturers (click here for PDF), EPA investigators found that the data the EPA now requires for registration do not accurately predict the toxicity when the product is approved and being widely used by consumers.
What does the term “Systemic” Mean?
Using vague and contradictory terminology, manufacturers imply that these chemicals are not absorbed into the dog’s system, but remain on the surface of the skin.
As an example, Merial Limited states that Frontline® (a phenylprazole insecticide) is “not systemically active,” but describes translocation (a change in location): that Frontline® is “gradually dispersed by the pet's natural oils, collecting in the oil glands in the skin… then wicked onto the hair over the next 30 days” (diffusion and capillary action; transfer from hair to hair as the dog moves); and “...Frontline® will not go into the bloodstream and hence very safe...” But this suggests an illogical conclusion: that fipronil (the “active” ingredient) remains in the sebaceous (oil) glands beneath the skin— and then leaves through the same entry point (to the hair) without moving into any other part of the dog’s body.
However, a 1996 EPA memorandum, “Review of Domestic Animal Safety Studies,” cites a study: “in which radio-labeled fipronil was administered to dogs… demonstrat(ing) that the chemical is absorbed systemically [into the bloodstream]. Plasma (intravascular fluid containing blood cells) levels of radioactivity were detected from day 2 to day 30 post-treatment.” Regarding packaging, the EPA concluded: “These statements (that “Fipronil is not absorbed into the body”) should be deleted from the label” (click to view PDF).
Fipronil has been linked to onset of “aggressive” behavior in adult dogs, and among other issues, autopsies have shown an accumulation of fipronil in canine livers and kidneys, causing an increase in organ weight. The EPA classifies fipronil as a carcinogen (produces cancer) because exposure to fipronil caused malignant thyroid tumors in laboratory animals.
What is “Adverse Drug Event” Reporting?
Premarket clearance trials are modeled and conducted by employees of the manufacturer
New generation ingestible (oral) pesticides (pills and “chews”) are classified as drugs, and thereby under purview of the US Food and Drug Administration (FDA). Consumers anticipate that the FDA ensures for advance planning and review for safety of these drugs. However, Consumer Safety Advocates, maintain that that confidence is badly misplaced, because both the US and international premarket clearance process is so meager. Clinical trials that are modeled, sponsored, and conducted by manufacturer employees are small: both in scope and number of test subjects (laboratory animals). Animals can be removed or adverse reactions excluded during tests in ways that skew or limit “results” favorable to government approval. The lab-based tests themselves are brief (six months), do not simulate “real-world” (or even in-home) circumstances, and incorporate an acknowledged defiance to examine long-term or chronic exposure to the drugs.
Manufacturers submit an employee-drafted list of viewed/observable adverse reactions noted during these trials, which become the reference thereafter for review. Veterinary professionals—who diagnose according to “observable clinical symptoms”—are thereby constrained by these exclusionary reports. Consumers whose dogs are injured or killed—sometimes violently or within hours of administering the drug—are confronted with these shortcomings: since the veterinarian refers to the manufacturer list which may be as brief as: “common side effects include (transient) vomiting, lethargy, loss of appetite…” Because of this framework, broad and serious adverse experiences are deflected from government or public scrutiny, and do not become part of the ongoing or cumulative record. The failed process is not only self-serving for the manufacturer, but self-perpetuating: because veterinarians are precluded from properly reporting. Consumers themselves are generally unaware
of its existence.
Pursuant to ensuring consumer safety, the FDA’s Center for Drug Evaluation and Research now collects information on adverse drug experiences that occur after a prescription medication (a drug) is approved or marketed. This postmarketing reporting (pharmacovigilance) is required by a 2007 revision to the FDA’s Food, Drug, and Cosmetic (FD&C) Act: (Chapter VII, SubChapter H, § 760). That Act established “adverse event reporting” requirements which apply to the manufacturers, packers, and distributors whose names appear on the labels of over-the-counter (OTC) or behind-the-counter (BTC) drugs marketed in the US.
The FDA’s Division of Compliance Risk Management and Surveillance (DCRM&S) is charged to enforce the Postmarketing Adverse Drug Experience (PADE) Reporting Requirements in an effort to ensure that the FDA is receiving data on rare, latent, or long-term drug effects that may not have been identified in premarket testing. The DCRM&S is responsible to confirm that PADE reports are accurate, complete, and submitted in a timely manner. Based on these reports, the division uses a risk-based approach to identify businesses and distributors for inspection and surveillance sampling to secure information related to public health. The inspections are evaluated to determine if regulatory action is necessary under the revised FD&C Act (Title 21 of the Code of Federal Regulations [CFR]).
The ADE reporting system depends on detection and voluntary self-reporting of adverse clinical events by veterinarians and dog/cat guardians. Consumer advocates stress that the ADE is the solitary official channel to impact review of a drug remaining on the market. In the case of veterinary drugs, the FDA’s Center for Veterinary Medicine (CVM) maintains a Cumulative Adverse Drug Event (ADE) Summaries database, intended to provide information on adverse effects that may not have been identified during pre-market testing of FDA approved animal drugs. As representative of the FDA's enforcement of the FD&C Act, the database, available online, has been criticized by food safety and consumer advocates as incomplete—fewer than 1 in 10 adverse events are actually reported—thereby inaccurate; and unreliable to the point of near meaninglessness.
CVM itself cautions that the reports are, in many instances, only a collection of data, citing, (among other issues) that:
- the quality of reporting affects usefulness of information;
- no information exists to determine the number of animals the drugs were prescribed and administered to (and that thereby, use of the reports to compare drugs is inappropriate);
- reporting is based on the “active ingredient” only; and
- most particularly, that widespread underreporting is likely.
Adverse drug experience reporting is the solitary official channel to impact review of a drug remaining on the market.
Government Standards: Five years... is “expeditious”?
In mid-March 2014, the U.S. EPA and two pet product companies announced an agreement to cease use of propoxur in flea collars. Propoxur is a (non-systemic) carbamate insecticide (derived from carbamic acid and act in a similar fashion as organophosphate insecticides) that kills by reversibly inactivating the enzyme acetylcholinesterase (AChE: essential to successful nerve function of arachnids). In agricultural use (on livestock) since 1959, it is known for fast knockdown and long residual effect (also highly toxic to certain species of birds). In 2009, the Natural Resources Defense Council (NRDC) filed a petition against the EPA for failing to disallow use of the toxic chemical despite that its status as a known neurotoxin and carcinogen (particularly: posing risk to brain and nervous system development in children) pursuant to California's “Proposition 65.”
a Slow Retreat
Under the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA), a pesticide cannot be sold that may cause adverse impacts to human health or the environment. Based on this standard, in 2007 NRDC petitioned the EPA to cancel (discontinue approval of manufacturer registrations) the use of propoxur in pet products. Flea& tick collars work by spreading insecticide on the animal’s fur. The principal route of entry for a carbamate poisoning is either by inhalation or ingestion; or secondarily by the dermal route. In 2009, NRDC released a research paper describing that high pesticide residue can remain on a dog’s or cat's fur for weeks after the collar is removed from the animal.
Pursuant to that report, NRDC also petitioned for cancellation of tetrachlorvinphos (TCVP: another common carbamate pesticide in the collars). The EPA issued an initial finding in 2010 that propoxur collars presented unacceptable exposure metrics, and completed a risk assessment in September 2013: indicating health issues “of concern” to children from exposure to the collars.
In February 2014, NRDC filed a federal lawsuit to force the EPA respond to their 2007 and 2009 petitions, citing earlier severe restrictions on household use of other known neurotoxic pesticides. Under the March 2014 cancellation agreement between the EPA, Sergeant’s Pet Care Products and Wellmark International (the two companies make products like Bansect®, Sentry®, Zodiac® and Biospot®), the companies would be allowed to continue producing collars containing propoxur until April 1, 2015, and to continue distributing them for an additional year. Subsequently, “The remaining products will go through the channels of trade until the existing stock of pet collars has been sold.” Despite acknowledged health threats and FIFRA stipulations, according to a statement issued by the EPA, “agreement with the registrants as outlined here would be the best way to remove these products from the marketplace in an expeditious manner.”
NRDC criticized this lengthy phase-out period as a “slow retreat,” noting also, that flea collars can sit on store shelves for years before they expire. As such, the products may remain in the marketplace for sale to consumers well after the 2016 date: a situation similar to that with Hartz’s Blockade® product in 1987. Carbaryl is still used in agricultural veterinary milieus. Further, the agreement did not address use of tetracholoinphos
in these products.
The Problem with “Synergists”
Piperonyl Butoxide (PBO) is a common factor of insecticide formulations with pyrethrins and a number of pyrethroids, including permethrin and tetramethrin products. The pyrethrins/pyrethroids are a class of organic compounds normally derived from Chrysanthemum cinerariifolium breeds that have potent insecticidal activity by targeting the nervous systems of insects.
Although it has no pesticidal action by itself, PBO is used as an insecticide synergist: since it enhances the potency of certain pesticides such as carbamates, pyrethrins, pyrethroids, and rotenone (from the seeds and stems of the jicama vine plant, and the roots of several members of Fabaceae). Combining PBO with insecticides can increase the effectiveness of another chemical by impeding breakdown, thereby increasing the time it holds its toxic properties.
PBO inhibits the insect’s natural defense mechanisms, most importantly, the Mixed Function Oxidase system (MFO: the cytochrome P-450 system, responsible for intracellular energy transfer). The MFO system is the primary route of detoxification in insects, enabling the oxidative breakdown of insecticides and synthetic pyrethroids. Evaluation of sub-chronic and chronic studies examining the toxicity of PBO have led the EPA to classify PBO as a possible “Group C” carcinogen, and studies have identified an association between prenatal exposure to PBOs to delays in neurodevelopment
Piperonyl Butoxide (PBO)?
“Premarket Clearance” doesn’t consider
The systemic nature of many antiparasitics makes the shortcomings in the premarket clearance process even more troubling, because long-term/chronic exposure is not considered when evaluating safety. As one example, the short duration of manufacturer research would not reveal liver damage, because only “acute” (visible) effects are noted. This approach is disregards the dog’s metabolic detoxification biochemistry and excludes the constant toxic burden that is contributing to the chronic disease epidemic veterinarians dog guardians and their veterinarians are coping with today.
The liver is the dog’s primary organ for detoxifying chemicals and metabolizing drugs. As it does so, the liver secretes bile that ends up back in the intestines. The liver also makes proteins important for blood clotting and other functions.
Enterohepatic circulation (EC) is the circulation of biliary acids, bilirubin, toxins or other substances from the liver to the bile, followed by entry into the small intestine, absorption by the enterocyte (intestinal adsorptive cells) and transport back to the liver. EC is an particularly important concept in the evaluation of veterinary anti-parasitics, because many of these pesticides or drugs (as lipophilic xenobiotics: not naturally produced by the dog himself) undergo this process causing repeated liver damage. EC means that some fragments which would not otherwise be toxic can become so because of this recycling process.
 Journal of Pesticide Reform v.17, n.3 Fall97; Northwest Coalition For Alternatives To Pesticides. See also: Reregistration Eligibility Decision (RED) for Permethrin, EPA 738-R-06-017, April 2006.
 Organophosphates are biochemicals, esters of phosphoric acid. Organophosphates are the basis of many insecticides, herbicides, and nerve gases, effective by irreversibly inactivating acetylcholinesterase, an enzyme which is essential to nerve function in insects, humans, and many animals. They can be absorbed through the lungs or skin, or by eating contaminated food. Studies indicate a possible link to adverse effects in the neurobehavioral development of fetuses and children, even at very low levels of exposure: research spanning decades identifies them as mutagents (genetic damage), as well as hormone and immune system disruptors. Organophosphates are widely used as solvents, plasticizers, and Ethylene Propylene (rubber) additives.
 Carbamates are organic compounds derived from carbamic acid: These insecticides (AchE) kill insects by reversibly inactivating the enzyme acetylcholinesteraste, terminating the transmission of nerve signals (see footnote 2, immediately above).
 FIFRA defines the term “unreasonable adverse effects on the environment” to mean: “(1) any unreasonable risk to man or the environment, taking into account the economic, social, and environmental costs and benefits of the use of any pesticide, or (2) a human dietary risk from residues that result from a use of a pesticide in or on any food inconsistent with the standard under section 408 of the Federal Food, Drug and Cosmetic Act.”
As an example: Imidacloprid’s mobility in soil has been demonstrated by a variety of studies. Despite the concern raised by these studies that imidacloprid may contaminate water, in 1994 EPA declined to classify it as Restricted Use Product: “We are not recommending that the turf and ornamental products be classified as restricted use products due to ground water concerns for several reasons. First, several of the proposed NTN products contain directions for use around the home and a Restricted Use Classification would not allow sale of these products to the homeowner. Second, professional lawn care companies will be users of these products and they will not use a Restricted Use Product.” It is clear that the decision was based not on scientific, but on economic considerations.
 Example: naphthalene, an “inert” in an imidacloprid product, showed clear evidence of cancer activity through inhalation (nasal cancers), as well as anemia, liver damage, cataracts, and skin allergies. An “inert” (unidentified) ingredient in the flea product Advantage® was implicated in the death of kittens who received doses within laboratory tolerances. (Kathleen Dudley, 2002: Are “Spot-On” Flea Killers Safe?).
 Status Report for PPDC, EPA. 1987. Inert ingredients in pesticide products; Policy statement. Fed. Reg. 52(77):13305, Apr. 22 (click here).
 Examples: head-nodding; facial twitching; exaggerated blinking; gag responses; weight increase of the spleen, thymus, and adrenal glands; and/or atrophy of the thymus.
 Wallinga & Greer, 2000: Poisons on Pets, Heath Hazards from Flea & Tick Products; NRDC.
We're knowable by look and even more so by our smells. Over and above that, how we act defines who we are. For dogs, the identity of a person not just how s/he smells and looks; it is how s/he moves.
We are recognizable by our behavior.
Even our most ordinary behavior, walking across a room in our characteristic style,
is chock full of information that the dog can mine. All dog owners watch their pups' growing sensitivity to the rituals that precede going for what in many dog peopled households is called a W-A-L-K.
And spelling that word instead of saying it is, of course, usually futile.
Dogs can also learn the connection between the cadence of a spelled word and a subsequent walk,
even if the latter does not immediately follow the former.
On the other hand, used in an unlikely context—say, sitting in the bath—
the spelled word will not evoke much interest.
Chances are slim you’re about to up and take a walk when naked and sudsy.
Dogs quickly learn to recognize shoe-donning, of course; we come to expect that grabbing a leash or a jacket
will clue them in; a regular walk time explains their prescience; but what if all you did was look up from your work or rise from your seat before you dog was on to you?
If done suddenly, or if you cross the room with a purposeful stride, an attentive dog has all the information he needs. Habitual watcher of your behavior, he sees your intent even when you think you are giving nothing away.
Dogs are very sensitive to gaze and thus to changes in our gaze. The difference between a head lifted up or angled down, away from them or toward them, is large for an animal so sensitive to eye contact. Even small movements of the hands or adjustments of the body attract notice.
Spend three hours looking at a computer screen, hands tethered to the keyboard... then look up and stretch your arms overhead—this is a metamorphosis!
The redirection of your intent is clear—and a hopeful dog can easily interpret it as a prelude to a walk.
An acute human observer would notice this too, but we rarely let others oversee us so closely in our daily affairs.”
—Alexandra Horowitz; Inside of a Dog